Undermind Research Topic: I want to find papers that investigate the molecular mechanism underlying Hebbian learning, including any involvement of hormone-like chemicals such as nerve growth factor.

Research topic

I want to find papers that investigate the molecular mechanism underlying Hebbian learning, including any involvement of hormone-like chemicals such as nerve growth factor.

Report

References

Last 5 years

Last 2 years

> 1 citation per year

> 5 citations per year

Topic Match

Cit./Year

Year

Paper

Paper Relevance Summary

97.6%

1.1

1999

[1] Activation of tyrosine receptor kinase plays a role in expression of long‐term potentiation in the rat dentate gyrus C. Maguire, ..., and M. Lynch Hippocampus 1999 - 29 citations - Show abstract - Cite 97.6% topic match

Demonstrates NGF's role in modulating LTP via tyrosine kinase. Shows NGF enhances glutamate release and calcium influx, involving trkA and ERK phosphorylation. Tyrosine kinase inhibitor blocks LTP and neurotransmitter release enhancements, confirming NGF's involvement in Hebbian mechanisms.

Demonstrates NGF's role in modulating LTP via tyrosine kinase. Shows NGF enhances glutamate release and calcium influx, involving trkA and ERK phosphorylation. Tyrosine kinase inhibitor blocks LTP and neurotransmitter release enhancements, confirming NGF's involvement in Hebbian mechanisms.

96.8%

11.9

2009

[2] NGF Is Essential for Hippocampal Plasticity and Learning J. Conner, ..., and M. Tuszynski The Journal of Neuroscience 2009 - 180 citations - Show abstract - Cite 96.8% topic match

Shows the role of NGF in hippocampal plasticity and learning. Demonstrates that NGF augmentation enhances LTP and cholinergic markers; blocking NGF impairs LTP and spatial memory retention. Explicitly links NGF to mechanisms underlying synaptic plasticity; pertinent to molecular mechanisms of Hebbian learning.

Shows the role of NGF in hippocampal plasticity and learning. Demonstrates that NGF augmentation enhances LTP and cholinergic markers; blocking NGF impairs LTP and spatial memory retention. Explicitly links NGF to mechanisms underlying synaptic plasticity; pertinent to molecular mechanisms of Hebbian learning.

96.0%

3.5

1994

[3] Short-term modulation of glutamatergic synapses in adult rat hippocampus by NGF. M. Knipper, ..., and Rylett Rj Neuroreport 1994 - 105 citations - Show abstract - Cite 96.0% topic match

Shows NGF's potentiation of glutamate release in hippocampal synapses. Describes NGF's effect on spontaneous/depolarization-evoked glutamate release, enhancing excitatory postsynaptic potentials in CA1 neurons. Reveals increased [32P]phosphate incorporation into synapsin I, illustrating a molecular mechanism for short-term synaptic modulation by NGF.

Shows NGF's potentiation of glutamate release in hippocampal synapses. Describes NGF's effect on spontaneous/depolarization-evoked glutamate release, enhancing excitatory postsynaptic potentials in CA1 neurons. Reveals increased [32P]phosphate incorporation into synapsin I, illustrating a molecular mechanism for short-term synaptic modulation by NGF.

94.3%

0.0

2009

[4] Effects of nerve growth factor on the organotypic hippocampal slice culture using MEA system Do-Hyoung Kim, ..., and I. Kim 2009 4th International IEEE/EMBS Conference on Neural Engineering 2009 - 0 citations - Show abstract - Cite 94.3% topic match

Investigates NGF effects on hippocampal slices using MEA system. Shows NGF-induced long-term potentiation (LTP)-like effects are mediated by TrkA receptors. Highly relevant due to focus on NGF's role in synaptic plasticity related to Hebbian mechanisms.

Investigates NGF effects on hippocampal slices using MEA system. Shows NGF-induced long-term potentiation (LTP)-like effects are mediated by TrkA receptors. Highly relevant due to focus on NGF's role in synaptic plasticity related to Hebbian mechanisms.

93.9%

0.0

2000

[5] NGF FASCILITATES HIPPOCAMPAL LTP AND IMPROVES MEMORY IN THE INTACT ADULT RAT BRAIN J. Conner, ..., and M.-H.-Tuszynski Journal Not Provided 2000 - 0 citations - Show abstract - Cite 93.9% topic match

Shows that NGF enhances hippocampal LTP and memory. Indicates NGF increases cholinergic neuron size, ChAT activity, and LTP induction in the hippocampus. Suggests a potential molecular mechanism by which NGF modulates hippocampal plasticity related to Hebbian learning.

Shows that NGF enhances hippocampal LTP and memory. Indicates NGF increases cholinergic neuron size, ChAT activity, and LTP induction in the hippocampus. Suggests a potential molecular mechanism by which NGF modulates hippocampal plasticity related to Hebbian learning.

93.3%

0.5

2004

[6] Nerve growth factor favours long‐term depression over long‐term potentiation in layer II–III neurones of rat visual cortex A. Brancucci, ..., and L. Domenici The Journal of Physiology 2004 - 10 citations - Show abstract - Cite 93.3% topic match

Shows NGF's effect on synaptic plasticity in the rat visual cortex. Demonstrates that NGF converts high-frequency stimulation-induced LTP into LTD in layer II–III neurons. Explores cellular-level mechanisms and directly involves NGF, pertinent to Hebbian learning research.

Shows NGF's effect on synaptic plasticity in the rat visual cortex. Demonstrates that NGF converts high-frequency stimulation-induced LTP into LTD in layer II–III neurons. Explores cellular-level mechanisms and directly involves NGF, pertinent to Hebbian learning research.

90.9%

1.4

1998

[7] Evidence that nerve growth factor plays a role in long-term potentiation in the rat dentate gyrus Á. Kelly, ..., and Marina A. Lynch Neuropharmacology 1998 - 37 citations - Show abstract - Cite 90.9% topic match

90.8%

8.2

1997

[8] Brain‐derived neurotrophic factor and nerve growth factor potentiate excitatory synaptic transmission in the rat visual cortex. G. Carmignoto, ..., and S. Vicini The Journal of Physiology 1997 - 227 citations - Show abstract - Cite 90.8% topic match

Shows the effects of BDNF and NGF on synaptic transmission. Demonstrates rapid increases in EPSC amplitude in rat visual cortex slices. Explicitly investigates NGF's role in excitatory synaptic transmission, relevant to Hebbian mechanisms.

Shows the effects of BDNF and NGF on synaptic transmission. Demonstrates rapid increases in EPSC amplitude in rat visual cortex slices. Explicitly investigates NGF's role in excitatory synaptic transmission, relevant to Hebbian mechanisms.

89.7%

1.3

2000

[9] Time‐dependent enhancement of inhibitory avoidance retention and MAPK activation by post‐training infusion of nerve growth factor into CA1 region of hippocampus of adult rats R. Walz, ..., and I. Izquierdo European Journal of Neuroscience 2000 - 31 citations - Show abstract - Cite 89.7% topic match

Shows: NGF enhances inhibitory avoidance retention via MAPK activation. Details: NGF infusion into CA1 hippocampus enhances IA retention and activates MAPK signaling post-training. Relevance: Directly investigates NGF's molecular role in synaptic plasticity, implicating MAPK signaling in Hebbian learning processes.

Shows: NGF enhances inhibitory avoidance retention via MAPK activation. Details: NGF infusion into CA1 hippocampus enhances IA retention and activates MAPK signaling post-training. Relevance: Directly investigates NGF's molecular role in synaptic plasticity, implicating MAPK signaling in Hebbian learning processes.

88.2%

0.6

1993

[10] Nerve growth factor inhibits the expression of long-term potentiation in hippocampal slices. V. Tancredi, ..., and P. Calissano Neuroreport 1993 - 18 citations - Show abstract - Cite 88.2% topic match

Shows NGF inhibiting LTP expression in the hippocampus. Details how exogenous NGF reduces LTP expression without altering basal synaptic transmission. Indicates NGF as a modulator of learning processes via high-affinity receptors.

Shows NGF inhibiting LTP expression in the hippocampus. Details how exogenous NGF reduces LTP expression without altering basal synaptic transmission. Indicates NGF as a modulator of learning processes via high-affinity receptors.

84.8%

4.7

1997

[11] Neurotrophin modulation of NMDA receptors in cultured murine and isolated rat neurons. C. R. Jarvis, ..., and J. Macdonald Journal of neurophysiology 1997 - 127 citations - Show abstract - Cite Abstract: Neurotrophin modulation of NMDA receptors in cultured murine and isolated rat neurons. J. Neurophysiol. 78: 2363-2371, 1997. Patch-clamp and calcium imaging techniques were used to assess the acute effects of the neurotrophins, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and nerve growth factor (NGF), on the responses of cultured and acutely isolated hippocampal and cultured striatal neurons to the glutamate receptor agonist N-methyl--aspartic acid (NMDA). The effects of BDNF on NMDA-activated currents were examined in greater detail. Currents evoked by NMDA, and the accompanying changes in intracellular calcium, were enhanced by low concentrations of the neurotrophins (1-20 ng/ml). The potentiation by the neurotrophins was rapid in onset and offset (<1 s). The neurotrophins also reduced desensitization of these currents in most cells. The enhancement of NMDA-activated currents by BDNF was observed using both perforated and whole cell patch recording techniques and could be demonstrated in outside-out patches. Furthermore, its effects were not attenuated by pretreatment with the protein kinase inhibitors genistein or 1-(5-isoquinolynesulfony)2-methylpiperazine (H7). Therefore, the actions of BDNF do not appear to be mediated by phosphorylation. Similar enhancements were observed with NT-3 and NT-4 and with NGF despite the fact that hippocampal neurons lack TrkA receptors. All together this evidence suggests that the enhancement of NMDA-evoked currents is unlikely to be mediated through the activation of growth factor receptors. Modulation of NMDA responses by BDNF was dependent on the concentration of extracellular glycine. The most pronounced potentiation by BDNF was observed at low concentrations, whereas no potentiation was observed in saturating concentrations of glycine, suggesting that BDNF may have increased the affinity of the NMDA receptor for glycine. However, the competitive glycine-site antagonist 7-chloro-kynurenic acid blocked the enhancement by BDNF without shifting the dose-inhibition relationship for this antagonist, and Mg2+ consistently depressed the potentiation of NMDA-evoked currents by BDNF, indicating that BDNF does not alter glycine affinity. BDNF also reversibly increased the probability of opening of NMDA channels recorded from outside-out patches taken from cultured hippocampal neurons. Other unrelated peptides including dynorphin and somatostatin also caused a glycine-dependent enhancement of NMDA currents and depressed the currents in saturating concentrations of glycine. In contrast, a shortened analogue dynorphin (6-17), which lacks N-terminus glycine residues, and another peptide met-enkephalin were without effects on NMDA currents recorded in low concentrations of glycine. Our results suggest that neurotrophins and other peptides can serve as glycine-like ligands for the NMDA receptor. 84.8% topic match

Shows how neurotrophins modulate NMDA receptor activity. Details the enhancement of NMDA-activated currents by NGF and other neurotrophins. Relevance: NGF's involvement in enhancing NMDA receptor function ties into molecular mechanisms of Hebbian learning.

Shows how neurotrophins modulate NMDA receptor activity. Details the enhancement of NMDA-activated currents by NGF and other neurotrophins. Relevance: NGF's involvement in enhancing NMDA receptor function ties into molecular mechanisms of Hebbian learning.

81.8%

2.2

1997

[12] Activation of calcium-dependent potassium channels in rat brain neurons by neurotrophin-3 and nerve growth factor N. R. Holm, ..., and S. Gammeltoft Proceedings of the National Academy of Sciences of the United States of America 1997 - 61 citations - Show abstract - Cite 81.8% topic match

Shows NGF activates calcium-dependent potassium channels in neurons. Details mechanism involving Trk tyrosine kinase, phospholipase C, and Ca2+ dependence. Explores neurotrophin effects on neuronal activity, relevant to understanding NGF's role in synaptic signaling pathways.

Shows NGF activates calcium-dependent potassium channels in neurons. Details mechanism involving Trk tyrosine kinase, phospholipase C, and Ca2+ dependence. Explores neurotrophin effects on neuronal activity, relevant to understanding NGF's role in synaptic signaling pathways.

81.0%

1.3

2012

[13] Nerve Growth Factor in the Hippocamposeptal System: Evidence for Activity-Dependent Anterograde Delivery and Modulation of Synaptic Activity Lan Guo, ..., and H. Yeh The Journal of Neuroscience 2012 - 16 citations - Show abstract - Cite 81.0% topic match

Examines NGF's role in hippocampal synaptic activity. Investigates activity-dependent anterograde delivery of NGF and its modulation of synaptic efficacy. Aligns with molecular mechanisms but does not explicitly discuss Hebbian learning.

Examines NGF's role in hippocampal synaptic activity. Investigates activity-dependent anterograde delivery of NGF and its modulation of synaptic efficacy. Aligns with molecular mechanisms but does not explicitly discuss Hebbian learning.

71.4%

0.5

2002

[14] Nerve growth factor enhances neurotransmitter release from PC12 cells by increasing Ca(2+)-responsible secretory vesicles through the activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase. S. Amino, ..., and Masami Takahashi Journal of biochemistry 2002 - 11 citations - Show abstract - Cite 71.4% topic match

Shows how NGF enhances neurotransmitter release via molecular pathways. Explores NGF's role in increasing Ca(2+)-responsive vesicles, involving MAPK and PI3K pathways. Relevant to NGF and synaptic mechanisms but may not directly link to Hebbian learning.

Shows how NGF enhances neurotransmitter release via molecular pathways. Explores NGF's role in increasing Ca(2+)-responsive vesicles, involving MAPK and PI3K pathways. Relevant to NGF and synaptic mechanisms but may not directly link to Hebbian learning.

71.3%

10.3

1993

[15] The induction of LTP increases BDNF and NGF mRNA but decreases NT-3 mRNA in the dentate gyrus. E. Castrén, ..., and P. Riekkinen Neuroreport 1993 - 321 citations - Show abstract - Cite 71.3% topic match

Investigates the expression of neurotrophic factor mRNAs after LTP induction. Shows bilateral increases in BDNF and NGF mRNAs in the dentate gyrus. Relevant as it links NGF expression changes to synaptic plasticity but lacks direct molecular mechanism details of Hebbian learning.

Investigates the expression of neurotrophic factor mRNAs after LTP induction. Shows bilateral increases in BDNF and NGF mRNAs in the dentate gyrus. Relevant as it links NGF expression changes to synaptic plasticity but lacks direct molecular mechanism details of Hebbian learning.

69.9%

3.6

1995

[16] Differential effects of NGF and BDNF on voltage-gated calcium currents in embryonic basal forebrain neurons E. Levine, ..., and M. Plummer Journal of Neuroscience 1995 - 106 citations - Show abstract - Cite 69.9% topic match

Shows effects of NGF and BDNF on calcium currents. Describes how NGF increases Ca(2+) channel currents in forebrain neurons, unlike BDNF. Indicates NGF's role in enhancing calcium entry, potentially relevant to molecular mechanisms of Hebbian learning.

Shows effects of NGF and BDNF on calcium currents. Describes how NGF increases Ca(2+) channel currents in forebrain neurons, unlike BDNF. Indicates NGF's role in enhancing calcium entry, potentially relevant to molecular mechanisms of Hebbian learning.

69.6%

10.9

2017

[17] Neurotrophins and Proneurotrophins: Focus on Synaptic Activity and Plasticity in the Brain J. Gibon and P. Barker The Neuroscientist 2017 - 83 citations - Show abstract - Cite 69.6% topic match

Explores neurotrophins in synaptic activity and plasticity Details roles of NGF, BDNF, NT3, and NT4 in LTP, LTD, and synaptic transmission Discusses NGF's involvement, aligning with the molecular mechanisms of Hebbian learning and hormone-like chemicals

Explores neurotrophins in synaptic activity and plasticity Details roles of NGF, BDNF, NT3, and NT4 in LTP, LTD, and synaptic transmission Discusses NGF's involvement, aligning with the molecular mechanisms of Hebbian learning and hormone-like chemicals

65.5%

4.9

1998

[18] Nerve growth factor and brain‐derived neurotrophic factor increase neurotransmitter release in the rat visual cortex R. Sala, ..., and L. Maffei European Journal of Neuroscience 1998 - 129 citations - Show abstract - Cite 65.5% topic match

Shows that NGF increases neurotransmitter release in the visual cortex. NGF enhances depolarization-evoked glutamate (≈90%) and acetylcholine (≈35%) release, not GABA, during the critical plasticity period. Indicates neurotrophin involvement in synaptic transmission modulation, focusing indirectly on the molecular mechanisms relevant to Hebbian learning.

Shows that NGF increases neurotransmitter release in the visual cortex. NGF enhances depolarization-evoked glutamate (≈90%) and acetylcholine (≈35%) release, not GABA, during the critical plasticity period. Indicates neurotrophin involvement in synaptic transmission modulation, focusing indirectly on the molecular mechanisms relevant to Hebbian learning.

65.1%

1.6

2002

[19] Nerve Growth Factor Enhances Neurotransmitter Release from PC12 Cells by Increasing Ca2+-Responsible Secretory Vesicles through the Activation of Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase S. Amino, ..., and Masami Takahashi Journal of Biochemistry 2002 - 35 citations - Show abstract - Cite 65.1% topic match

Shows that NGF enhances neurotransmitter release from PC12 cells. Increases Ca2+-responsive secretory vesicles through PI 3-kinase and MAP kinase activation. Relevant for understanding NGF's molecular role in synaptic modulation, but lacks direct link to Hebbian learning mechanisms.

Shows that NGF enhances neurotransmitter release from PC12 cells. Increases Ca2+-responsive secretory vesicles through PI 3-kinase and MAP kinase activation. Relevant for understanding NGF's molecular role in synaptic modulation, but lacks direct link to Hebbian learning mechanisms.

63.3%

2.8

2000

[20] BDNF, NT‐3 and NGF induce distinct new Ca2+ channel synthesis in developing hippocampal neurons P. Baldelli, ..., and E. Carbone European Journal of Neuroscience 2000 - 68 citations - Show abstract - Cite 63.3% topic match

Shows neurotrophins' influence on Ca2+ channel synthesis. Demonstrates NGF, BDNF, NT-3 induce Ca2+ channel up-regulation in hippocampal neurons. NGF up-regulates L-currents, relevant for Hebbian synaptic plasticity mechanisms involving intracellular Ca2+.

Shows neurotrophins' influence on Ca2+ channel synthesis. Demonstrates NGF, BDNF, NT-3 induce Ca2+ channel up-regulation in hippocampal neurons. NGF up-regulates L-currents, relevant for Hebbian synaptic plasticity mechanisms involving intracellular Ca2+.

58.8%

1.5

1999

[21] Effects of nerve growth factor on visual cortical plasticity require afferent electrical activity M. Caleo, ..., and L. Maffei European Journal of Neuroscience 1999 - 37 citations - Show abstract - Cite 58.8% topic match

Shows the role of NGF in cortical plasticity. NGF signaling via TrkA requires afferent electrical activity to affect neuron eye preference. Relevant to NGF's involvement but focuses on visual cortex, not directly on Hebbian mechanisms.

Shows the role of NGF in cortical plasticity. NGF signaling via TrkA requires afferent electrical activity to affect neuron eye preference. Relevant to NGF's involvement but focuses on visual cortex, not directly on Hebbian mechanisms.

57.5%

0.1

2011

[22] Ligand-dependent TrkA activity in brain impacts differently on spatial learning and long-term memory Tahar Aboulkassim, ..., and H. U. Saragovi Journal Not Provided 2011 - 1 citations - Show abstract - Cite 57.5% topic match

Investigates TrkA activation's impact on learning and memory. Shows TrkA activation improves learning and short-term memory in APP mice but not long-term memory. Highlights TrkA selective agonists' role without extensive focus on molecular mechanisms underlying Hebbian learning or involvement of NGF-specific molecular pathways.

Investigates TrkA activation's impact on learning and memory. Shows TrkA activation improves learning and short-term memory in APP mice but not long-term memory. Highlights TrkA selective agonists' role without extensive focus on molecular mechanisms underlying Hebbian learning or involvement of NGF-specific molecular pathways.

56.7%

5.1

1996

[23] Unilateral LTP triggers bilateral increases in hippocampal neurotrophin and trk receptor mRNA expression in behaving rats: Evidence for interhemispheric communication C. Bramham, ..., and L. Brady Journal of Comparative Neurology 1996 - 146 citations - Show abstract - Cite 56.7% topic match

Shows NGF and trk receptor mRNA upregulation during LTP in hippocampal neurons. Induction of LTP in awake rats increased NGF, BDNF, NT-3, trkB, and trkC mRNA levels. Relevant as it discusses NGF and neurotrophin expression linked to synaptic plasticity, but focus is on general LTP, not specifically Hebbian learning.

Shows NGF and trk receptor mRNA upregulation during LTP in hippocampal neurons. Induction of LTP in awake rats increased NGF, BDNF, NT-3, trkB, and trkC mRNA levels. Relevant as it discusses NGF and neurotrophin expression linked to synaptic plasticity, but focus is on general LTP, not specifically Hebbian learning.

56.3%

0.6

1998

[24] Nerve growth factor rapidly suppresses basal, NMDA-evoked, and AMPA-evoked nitric oxide synthase activity in rat hippocampus in vivo. H. H. Lam, ..., and M. Sofroniew Proceedings of the National Academy of Sciences of the United States of America 1998 - 16 citations - Show abstract - Cite 56.3% topic match

Shows NGF's rapid suppression of nitric oxide synthase (NOS) activity. Demonstrates NGF impacts NMDA- and AMPA-induced NOS activity in rat hippocampus locally, not solely via retrograde transport. Highlights a potential NGF-mediated mechanism relevant to synaptic activity and plasticity, but does not directly discuss Hebbian learning mechanisms.

Shows NGF's rapid suppression of nitric oxide synthase (NOS) activity. Demonstrates NGF impacts NMDA- and AMPA-induced NOS activity in rat hippocampus locally, not solely via retrograde transport. Highlights a potential NGF-mediated mechanism relevant to synaptic activity and plasticity, but does not directly discuss Hebbian learning mechanisms.

56.2%

0.0

1998

[25] Nerve growth factor acutely reduces chemical transmission by means of postsynaptic TrkA-like receptors in squid giant synapse (neurotrophins and neurotrophisysynaptic transmissionypresynapticyphosphorylationyautophosphorylation) H. Moreno, ..., and J. Schlessinger Journal Not Provided 1998 - 1 citations - Show abstract - Cite 56.2% topic match

Shows NGF reduces postsynaptic potential via TrkA-like receptors. NGF triggers tyrosine phosphorylation at postsynaptic sites in squid giant synapse, indicating receptor tyrosine kinase activation and postsynaptic modulation. Article focuses on synaptic transmission modulation rather than on Hebbian learning mechanisms directly.

Shows NGF reduces postsynaptic potential via TrkA-like receptors. NGF triggers tyrosine phosphorylation at postsynaptic sites in squid giant synapse, indicating receptor tyrosine kinase activation and postsynaptic modulation. Article focuses on synaptic transmission modulation rather than on Hebbian learning mechanisms directly.

55.5%

0.6

1998

[26] Nerve growth factor acutely reduces chemical transmission by means of postsynaptic TrkA-like receptors in squid giant synapse. H. Moreno, ..., and R. Llinás Proceedings of the National Academy of Sciences of the United States of America 1998 - 15 citations - Show abstract - Cite 55.5% topic match

Provides insights into NGF's role in synaptic transmission. Shows that NGF reduces postsynaptic potential amplitude through TrkA-like receptors in squid synapse. This suggests NGF modulates synaptic plasticity, indirectly relevant to Hebbian learning mechanisms.

Provides insights into NGF's role in synaptic transmission. Shows that NGF reduces postsynaptic potential amplitude through TrkA-like receptors in squid synapse. This suggests NGF modulates synaptic plasticity, indirectly relevant to Hebbian learning mechanisms.

55.4%

3.1

2008

[27] Chronic Exposure to Nerve Growth Factor Increases Acetylcholine and Glutamate Release from Cholinergic Neurons of the Rat Medial Septum and Diagonal Band of Broca via Mechanisms Mediated by p75NTR Carey Y. L. Huh, ..., and Sylvain Williams The Journal of Neuroscience 2008 - 51 citations - Show abstract - Cite 55.4% topic match

Shows NGF's effect on synaptic transmission in cholinergic neurons. Demonstrates that chronic NGF exposure boosts acetylcholine and glutamate release via p75NTR in MS-DBB neurons. Focuses on synaptic function, potentially relevant due to NGF's involvement, but does not directly address Hebbian mechanisms.

Shows NGF's effect on synaptic transmission in cholinergic neurons. Demonstrates that chronic NGF exposure boosts acetylcholine and glutamate release via p75NTR in MS-DBB neurons. Focuses on synaptic function, potentially relevant due to NGF's involvement, but does not directly address Hebbian mechanisms.

54.7%

1.7

2000

[28] Differential effects of neurotrophins on ocular dominance plasticity in developing and adult cat visual cortex R. Galuske, ..., and W. Singer European Journal of Neuroscience 2000 - 42 citations - Show abstract - Cite 54.7% topic match

Examines the influence of neurotrophins on synaptic plasticity. Specifically investigates BDNF and NGF effects on ocular dominance plasticity in visual cortex. Uses optical and electrophysiological techniques to assess cortical architecture changes during development and adulthood.

Examines the influence of neurotrophins on synaptic plasticity. Specifically investigates BDNF and NGF effects on ocular dominance plasticity in visual cortex. Uses optical and electrophysiological techniques to assess cortical architecture changes during development and adulthood.

52.7%

3.0

2001

[29] Elevation of Nerve Growth Factor and Antisense Knockdown of TrkA Receptor during Contextual Memory Consolidation N. Woolf, ..., and A. Roghani The Journal of Neuroscience 2001 - 72 citations - Show abstract - Cite 52.7% topic match

Shows NGF's Role in Contextual Memory Consolidation. Reveals increased NGF levels in the hippocampus 1 week post-training. Mentions TrkA receptor involvement but does not specify Hebbian learning.

Shows NGF's Role in Contextual Memory Consolidation. Reveals increased NGF levels in the hippocampus 1 week post-training. Mentions TrkA receptor involvement but does not specify Hebbian learning.

52.3%

3.0

2001

[30] Nerve Growth Factor Rapidly Induces Prolonged Acetylcholine Release from Cultured Basal Forebrain Neurons: Differentiation between Neuromodulatory and Neurotrophic Influences D. Auld, ..., and R. Quirion The Journal of Neuroscience 2001 - 70 citations - Show abstract - Cite 52.3% topic match

Shows NGF's impact on ACh release in basal forebrain neurons. Demonstrates activity-dependent, LTP-like enhancement of ACh release via TrkA and Ca2+ pathways. Highlights potential neuromodulatory and neurotrophic mechanisms but lacks direct focus on Hebbian learning.

Shows NGF's impact on ACh release in basal forebrain neurons. Demonstrates activity-dependent, LTP-like enhancement of ACh release via TrkA and Ca2+ pathways. Highlights potential neuromodulatory and neurotrophic mechanisms but lacks direct focus on Hebbian learning.

51.1%

3.6

1996

[31] Brain‐derived Neurotrophic Factor Reverses Experience‐dependent Synaptic Modifications in Kitten Visual Cortex R. Galuske, ..., and W. Singer European Journal of Neuroscience 1996 - 103 citations - Show abstract - Cite 51.1% topic match

Investigates the effect of NGF on synaptic modifications. Examines synaptic responses in kitten visual cortex with NGF infusion under monocular deprivation. Finds NGF has no impact on modifying synaptic changes induced by visual deprivation.

Investigates the effect of NGF on synaptic modifications. Examines synaptic responses in kitten visual cortex with NGF infusion under monocular deprivation. Finds NGF has no impact on modifying synaptic changes induced by visual deprivation.

50.9%

14.6

1992

[32] Nerve growth factor mediates signal transduction through trk homodimer receptors Shuqian Jing, ..., and M. Barbacid Neuron 1992 - 467 citations - Show abstract - Cite 50.9% topic match

48.5%

8.2

1992

[33] Nerve growth factor (NGF) prevents the shift in ocular dominance distribution of visual cortical neurons in monocularly deprived rats L. Maffei, ..., and T. Pizzorusso Journal of Neuroscience 1992 - 260 citations - Show abstract - Cite 48.5% topic match

Shows NGF's role in visual cortical plasticity under monocular deprivation conditions. Indicates exogenous NGF prevents changes in ocular dominance in monocularly deprived rats. Relevant to synaptic plasticity modulation by NGF but lacks direct linkage to Hebbian learning mechanisms.

Shows NGF's role in visual cortical plasticity under monocular deprivation conditions. Indicates exogenous NGF prevents changes in ocular dominance in monocularly deprived rats. Relevant to synaptic plasticity modulation by NGF but lacks direct linkage to Hebbian learning mechanisms.

40.6%

46.9

1995

[34] Long-lasting neurotrophin-induced enhancement of synaptic transmission in the adult hippocampus Hyejin Kang and E. Schuman Science 1995 - 1389 citations - Show abstract - Cite 40.6% topic match

Paper shows: NGF has no significant effect on synaptic strength in hippocampus. Details: BDNF and NT-3 dramatically enhance synaptic strength; NGF does not, indicating differential roles in plasticity. Additional info: This paper is somewhat related; it addresses synaptic plasticity but not Hebbian learning mechanisms or NGF's specific role in such.

Paper shows: NGF has no significant effect on synaptic strength in hippocampus. Details: BDNF and NT-3 dramatically enhance synaptic strength; NGF does not, indicating differential roles in plasticity. Additional info: This paper is somewhat related; it addresses synaptic plasticity but not Hebbian learning mechanisms or NGF's specific role in such.

38.9%

0.4

1997

[35] Trophic Factors, Synaptic Pasticity, and Memory E. Levine and I. Black Annals of the New York Academy of Sciences 1997 - 11 citations - Show abstract - Cite Abstract: One of the central issues in neuroscience concerns the cellular foundations of memory. How are brief environmental experiences translated into stable, longlasting changes in brain function? Conversely, how are learning and memory processes disrupted by degenerative disease or injury? At a mechanistic level, this is a question of how brain activity itself modifies the functional connections between neurons, the synapses. Activity-dependent modulation of synaptic transmission has assumed primacy in most formulations of memory. The synaptic apparatus simultaneously subserves millisecond-to-millisecond interneuronal communication and stores long-term information, thereby participating in the mnemonic process. Although there is an ever-expanding list of transmitters, peptides, and hormones that function as synaptic messengers, little is known about the intercellular signals that regulate the strength and efficacy of synaptic transmission. One potentially rewarding approach is to focus on the signals that regulate nervous system development, when maximal synaptic and neural plasticity occurs. During development, the functional circuitry of the brain is established through processes of axonal and dendritic outgrowth, synapse formation and stabilization, and the loss of neurons that fail to make appropriate connections. Growth and trophic factors are important classes of signals involved in these events. In particular, nerve growth factor (NGF) and related neurotrophins are essential for the selective survival and differentiation of specific neurons within the peripheral and central nervous systems.'2 In this brief overview, we focus on our recent studies suggesting a novel role for these trophic factors in the dynamic modulation of synaptic efficacy, both during development and in maturity. Most importantly, trophins acutely modulate both preand postsynaptic mechanisms regulating synaptic transmission. Additionally, trophin gene expression itself is regulated by neuronal impulse activity, indicating that external stimuli modulate trophin availability. Thus, signaling mechanisms that participate in the formation of neuronal circuits during development appear to operate throughout life to modulate interneuronal communication. The neurotrophin gene family includes NGF, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-415). Three trk family members, trkA, trkB, and trkC, encode essential components of receptors for these neurotrophins? NGF acts upon trkA, BDNF and NT-4/5 on trkB, and NT-3 acts primarily on trkC, but also interacts with trkA and trkB.3-5 All neurotrophins also bind to p75, a widely distributed receptor of uncertain functiom6 Neurotrophin 38.9% topic match

Provides insights on trophic factors, including NGF, in synaptic plasticity. Discusses NGF's role in brain development and synaptic modulation during memory processes. Focuses broadly on synaptic plasticity, not specifically on Hebbian learning mechanisms.

Provides insights on trophic factors, including NGF, in synaptic plasticity. Discusses NGF's role in brain development and synaptic modulation during memory processes. Focuses broadly on synaptic plasticity, not specifically on Hebbian learning mechanisms.

38.7%

8.7

1997

[36] Role of Neurotrophins in Synapse Development and Plasticity B. Lu and A. Figurov Reviews in the Neurosciences 1997 - 242 citations - Show abstract - Cite 38.7% topic match

Investigates neurotrophins and synaptic plasticity. Highlights BDNF's role in LTP, a key element of synaptic plasticity. Does not specifically address NGF or Hebbian learning mechanisms.

Investigates neurotrophins and synaptic plasticity. Highlights BDNF's role in LTP, a key element of synaptic plasticity. Does not specifically address NGF or Hebbian learning mechanisms.

37.9%

2.0

2000

[37] Afferent‐specific modulation of short‐term synaptic plasticity by neurotrophins in dentate gyrus F. Asztely, ..., and O. Lindvall European Journal of Neuroscience 2000 - 50 citations - Show abstract - Cite 37.9% topic match

Shows modulation of synaptic plasticity by neurotrophins in the dentate gyrus. Details how BDNF and NT-3 affect LPP and MPP differently. Does not explicitly focus on Hebbian learning or NGF involvement.

Shows modulation of synaptic plasticity by neurotrophins in the dentate gyrus. Details how BDNF and NT-3 affect LPP and MPP differently. Does not explicitly focus on Hebbian learning or NGF involvement.

34.8%

3.3

2011

[38] Ligand-Dependent TrkA Activity in Brain Differentially Affects Spatial Learning and Long-Term Memory Tahar Aboulkassim, ..., and Rosalind Franklin Molecular Pharmacology 2011 - 44 citations - Show abstract - Cite 34.8% topic match

Shows that TrkA activation affects learning and memory. Demonstrates that selective TrkA agonists improve short-term memory in transgenic mice. Does not specifically address Hebbian learning mechanisms or molecular pathways involving NGF and synaptic tagging.

Shows that TrkA activation affects learning and memory. Demonstrates that selective TrkA agonists improve short-term memory in transgenic mice. Does not specifically address Hebbian learning mechanisms or molecular pathways involving NGF and synaptic tagging.

33.8%

None

[39] Edinburgh Research Explorer Msk1 Regulates Homeostatic and Experience-dependent Synaptic Plasticity Msk1 Regulates Homeostatic and Experience-dependent Synaptic Plasticity Sonia A. L. Corrêa, ..., and B. Frenguelli Journal Not Provided None - 0 citations - Show abstract - Cite Abstract: General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact openaccess@ed.ac.uk providing details, and we will remove access to the work immediately and investigate your claim. The ability of neurons to modulate synaptic strength underpins synaptic plasticity, learning and memory, and adaptation to sensory experience. Despite the importance of synaptic adaptation in directing, reinforcing, and revising the behavioral response to environmental influences, the cellular and molecular mechanisms underlying synaptic adaptation are far from clear. Brain-derived neurotrophic factor (BDNF) is a prime initiator of structural and functional synaptic adaptation. However, the signaling cascade activated by BDNF to initiate these adaptive changes has not been elucidated. We have previously shown that BDNF activates mitogen-and stress-activated kinase 1 (MSK1), which regulates gene transcription via the phosphorylation of both CREB and histone H3. Using mice with a kinase-dead knock-in mutation of MSK1, we now show that MSK1 is necessary for the upregulation of synaptic strength in response to environmental enrichment in vivo. Furthermore, neurons from MSK1 kinase-dead mice failed to show scaling of synaptic transmission in response to activity deprivation in vitro, a deficit that could be rescued by reintroduction of wild-type MSK1. We also show that MSK1 forms part of a BDNF-and MAPK-dependent signaling cascade required for homeostatic synaptic scaling, which likely resides in the ability of MSK1 to regulate cell surface GluA1 expression via the induction of Arc/Arg3.1. These results demonstrate that MSK1 is an integral part of a signaling pathway that underlies the adaptive response to synaptic and environmental experience. MSK1 may thus act as a key homeostat in the activity-and experience-dependent regulation of synaptic strength. 33.8% topic match

Examines: BDNF's role in synaptic plasticity via MSK1 activation. Details: BDNF activates MSK1 to regulate gene transcription by phosphorylating CREB and histone H3, influencing synaptic adaptation. Relevance: Though it explores molecular mechanisms, the focus is on BDNF rather than NGF in Hebbian learning.

Examines: BDNF's role in synaptic plasticity via MSK1 activation. Details: BDNF activates MSK1 to regulate gene transcription by phosphorylating CREB and histone H3, influencing synaptic adaptation. Relevance: Though it explores molecular mechanisms, the focus is on BDNF rather than NGF in Hebbian learning.

31.7%

1.5

1999

[40] Nerve Growth Factor (NGF)-induced Calcium Influx and Intracellular Calcium Mobilization in 3T3 Cells Expressing NGF Receptors* Hao Jiang, ..., and G. Guroff The Journal of Biological Chemistry 1999 - 38 citations - Show abstract - Cite 31.7% topic match

Investigates NGF-induced calcium dynamics in 3T3 cells. Explores how NGF regulates calcium uptake and mobilization via high and low affinity NGF receptors. Focuses on mechanisms in 3T3 cells, relevance to Hebbian learning in neurons is indirect.

Investigates NGF-induced calcium dynamics in 3T3 cells. Explores how NGF regulates calcium uptake and mobilization via high and low affinity NGF receptors. Focuses on mechanisms in 3T3 cells, relevance to Hebbian learning in neurons is indirect.

30.9%

0.2

2016

[41] Molecular mechanisms of synaptic plasticity Hongik Hwang Journal Not Provided 2016 - 2 citations - Show abstract - Cite 30.9% topic match

Focuses on the molecular mechanisms of synaptic plasticity. Emphasizes the role of calmodulin and neurogranin in regulating intracellular calcium. Does not mention Hebbian learning or nerve growth factor (NGF).

Focuses on the molecular mechanisms of synaptic plasticity. Emphasizes the role of calmodulin and neurogranin in regulating intracellular calcium. Does not mention Hebbian learning or nerve growth factor (NGF).

30.8%

26.1

2003

[42] Brain-derived neurotrophic factor/TrkB signaling in memory processes. Kiyofumi Yamada and T. Nabeshima Journal of pharmacological sciences 2003 - 563 citations - Show abstract - Cite 30.8% topic match

Shows the role of BDNF/TrkB signaling in memory processes. Discusses activity-dependent synaptic plasticity, highlighting mechanisms like PI3-K and MAPK pathways. Does not mention nerve growth factor (NGF) or specific Hebbian learning mechanisms, focusing instead on BDNF-related pathways.

Shows the role of BDNF/TrkB signaling in memory processes. Discusses activity-dependent synaptic plasticity, highlighting mechanisms like PI3-K and MAPK pathways. Does not mention nerve growth factor (NGF) or specific Hebbian learning mechanisms, focusing instead on BDNF-related pathways.

30.2%

11.1

1997

[43] Brain-derived neurotrophic factor rapidly enhances phosphorylation of the postsynaptic N-methyl-D-aspartate receptor subunit 1. Piin-chau Suen, ..., and I. Black Proceedings of the National Academy of Sciences of the United States of America 1997 - 303 citations - Show abstract - Cite 30.2% topic match

Shows BDNF enhances phosphorylation of NMDA receptor subunit 1. Demonstrates rapid, dose-dependent effect via TrkB in hippocampal neurons. NGF does not affect phosphorylation, focusing BDNF's unique role in synaptic plasticity.

Shows BDNF enhances phosphorylation of NMDA receptor subunit 1. Demonstrates rapid, dose-dependent effect via TrkB in hippocampal neurons. NGF does not affect phosphorylation, focusing BDNF's unique role in synaptic plasticity.

29.8%

0.6

1992

[44] Intracellular calcium levels regulate the actions of nerve growth factor on calcium uptake in PC12 cells A. Kozak, ..., and G. Guroff Journal of Neuroscience Research 1992 - 19 citations - Show abstract - Cite 29.8% topic match

Shows the regulation of NGF on calcium uptake in PC12 cells. NGF stimulates divalent cation uptake and increases intracellular calcium, influenced by initial calcium levels. While relevant to NGF and Ca2+ dynamics, it does not directly address Hebbian learning mechanisms.

Shows the regulation of NGF on calcium uptake in PC12 cells. NGF stimulates divalent cation uptake and increases intracellular calcium, influenced by initial calcium levels. While relevant to NGF and Ca2+ dynamics, it does not directly address Hebbian learning mechanisms.

28.4%

2.0

2010

[45] Neurogranin and synaptic plasticity balance Ling Zhong and N. Gerges Communicative & Integrative Biology 2010 - 29 citations - Show abstract - Cite 28.4% topic match

Shows the role of neurogranin in synaptic plasticity. Neurogranin enhances synaptic strength in an NMDA receptor-dependent, activity-dependent manner. Does not address hormone-like chemicals or nerve growth factor.

Shows the role of neurogranin in synaptic plasticity. Neurogranin enhances synaptic strength in an NMDA receptor-dependent, activity-dependent manner. Does not address hormone-like chemicals or nerve growth factor.

27.1%

1.4

2019

[46] Nerve growth factor catches copper in neuronal inning D. La Mendola Neural Regeneration Research 2019 - 7 citations - Show abstract - Cite Abstract: The physiological effect of neurotrophic factors and their role in Alzheimer’s disease (AD): Neurotrophins (NTs) are a family of homologues proteins that play an essential role in neuronal cells growth, survival and differentiation. These proteins include the nerve growth factor (NGF), the brain derived neurotrophic factor (BDNF), NT-3 and NT-3, also known as NT-4/5. The biological functions of NTs are regulated by binding to two distinct classes of receptors, namely p75 neurotrophin receptor and tropomyosin receptor kinase (Trk). p75 neurotrophin receptor is member of the tumour necrosis factor receptor family, which binds with no selectivity all of the neurotrophins. On the other hand, to each NT there is a specific Trk receptor: NGF binds to TrkA, BDNF and NT-4 to TrkB, NT-3 interacts mainly with TrkC, respectively (Bothwell, 2014). NGF is the first discovered and best-characterized member of NTs family. Similarly to all the other neurotrophic factors, NGF is synthesized in a precursor form (pro-NGF) and is cleaved by proteases (e.g., plasmin, furin, matrix metalloproteinase (MMP7 and MMP3) to produce the mature and active form, which typically exerts its biological action as non-covalent homodimer. The cholinergic system of the human brain is considered as the master regulator of mnemonic functions and its loss is strictly associated with the cognitive decline (Cuello et al., 2019). NGF is secreted by post-synaptic target tissues and it is known to activate, by the binding to TrkA receptor, the signaling pathways at the axonal growth cones. Retrograde NGF transport maintains the phenotype of basal forebrain cholinergic neurons and control the long distance communication between the axon terminals and the neuronal cell bodies. Specifically, NGF binding to TrkA activates the three following signaling pathways: i) the phosphatidylinositol 3-kinase/protein kinase B (Akt); ii) the Ras/mitogen-activated protein kinase (ERK) and iii) the phospholipase C. In particular, the ERK or Akt pathways trigger the phosphorylation of transcription factor cAMP response element binding protein (CREB). This, in turn, induces the expression of proteins, including BDNF, which are directly involved in memory formation and consolidation. Noteworthy, NGF metabolism is hampered in AD, thus determining a widespread loss of cholinergic neurons in the basal forebrain with consequent loss in cognition and memory. NGF signalling pathways control also the post-translational modifications of the amyloid precursor protein (APP) and the amyloid beta (Aβ) production in neurons. Indeed, the deprivation in NGF determines Aβ aggregation and tau hyperphosphorylation (Canu et al., 2017). BDNF can reduce the production of toxic Aβ oligomers through a mechanism that increases α-secretase processing of APP. It has been often reported that different NTs perform similar activities in physiological as well as pathological conditions. However, the levels of NGF and BDNF follow different trend in hippocampus of AD animal models: at early stages of pathology, Aβ oligomers lead to significant reductions in BDNF expression whereas, at later stages, deficits in the NGF metabolic pathway occur. 27.1% topic match

Explores NGF-mediated signaling pathways relevant to neuronal function. Details how NGF binding to TrkA activates PI3K/Akt, Ras/MAPK, and PLC pathways. Focuses on NGF signaling, not explicitly discussing Hebbian learning mechanisms or synaptic plasticity.

Explores NGF-mediated signaling pathways relevant to neuronal function. Details how NGF binding to TrkA activates PI3K/Akt, Ras/MAPK, and PLC pathways. Focuses on NGF signaling, not explicitly discussing Hebbian learning mechanisms or synaptic plasticity.

26.7%

7.5

1991

[47] Nerve growth factor rapidly stimulates tyrosine phosphorylation of phospholipase C-gamma 1 by a kinase activity associated with the product of the trk protooncogene. M. Vetter, ..., and D. Kaplan Proceedings of the National Academy of Sciences of the United States of America 1991 - 251 citations - Show abstract - Cite 26.7% topic match

Shows NGF stimulates tyrosine phosphorylation via Trk-related kinase activity. Details the activation and phosphorylation of PLC-gamma 1 by NGF in PC12 cells. Focuses on NGF signaling; does not specify the involvement in Hebbian learning.

Shows NGF stimulates tyrosine phosphorylation via Trk-related kinase activity. Details the activation and phosphorylation of PLC-gamma 1 by NGF in PC12 cells. Focuses on NGF signaling; does not specify the involvement in Hebbian learning.

26.2%

4.9

2004

[48] Synaptic homeostasis and input selectivity follow from a calcium-dependent plasticity model. L. Yeung, ..., and L. Cooper Proceedings of the National Academy of Sciences of the United States of America 2004 - 98 citations - Show abstract - Cite 26.2% topic match

Describes a calcium-dependent plasticity model for Hebbian learning. Explores the role of NMDAR-mediated calcium currents in synaptic strength modifications. Does not specifically discuss nerve growth factor or hormone-like chemicals.

Describes a calcium-dependent plasticity model for Hebbian learning. Explores the role of NMDAR-mediated calcium currents in synaptic strength modifications. Does not specifically discuss nerve growth factor or hormone-like chemicals.

26.0%

0.4

1996

[49] Neurotrophins and the Synapse S. Finkbeiner The Neuroscientist 1996 - 12 citations - Show abstract - Cite 26.0% topic match

Shows how neurotrophins-modulate synaptic plasticity. Describes rapid and lasting synaptic efficacy changes induced by neurotrophins. Does not specifically address Hebbian learning or NGF.

Shows how neurotrophins-modulate synaptic plasticity. Describes rapid and lasting synaptic efficacy changes induced by neurotrophins. Does not specifically address Hebbian learning or NGF.

24.5%

4.7

2016

[50] Control of Ca2+ Influx and Calmodulin Activation by SK-Channels in Dendritic Spines Thom Griffith, ..., and J. Mellor PLoS Computational Biology 2016 - 40 citations - Show abstract - Cite 24.5% topic match

Examines how SK-channels control Ca2+ influx and calmodulin activation. Details how SK-channels regulate the magnitude of [Ca2+] increases by NMDA and VGCC activation. Does not address hormone-like chemicals or neurotrophic factors like nerve growth factor, focusing only on ion channel regulation mechanisms.

Examines how SK-channels control Ca2+ influx and calmodulin activation. Details how SK-channels regulate the magnitude of [Ca2+] increases by NMDA and VGCC activation. Does not address hormone-like chemicals or neurotrophic factors like nerve growth factor, focusing only on ion channel regulation mechanisms.

24.4%

1.3

2019

[51] Pharmacological interrogation of TrkA-mediated mechanisms in hippocampal-dependent memory consolidation S. Josephy-Hernandez, ..., and H. Saragovi PLoS ONE 2019 - 7 citations - Show abstract - Cite 24.4% topic match

Investigates TrkA-mediated mechanisms in memory consolidation. Explores effects of TrkA agonist D3 on hippocampal-dependent memory. Does not directly address Hebbian learning or explicitly involve NGF in a synaptic plasticity context.

Investigates TrkA-mediated mechanisms in memory consolidation. Explores effects of TrkA agonist D3 on hippocampal-dependent memory. Does not directly address Hebbian learning or explicitly involve NGF in a synaptic plasticity context.

24.0%

12.2

2006

[52] Brain-derived neurotrophic factor mechanisms and function in adult synaptic plasticity: new insights and implications for therapy. S. Kuipers and C. Bramham Current opinion in drug discovery & development 2006 - 221 citations - Show abstract - Cite 24.0% topic match

Focuses on BDNF's role in synaptic plasticity. Discusses BDNF mechanisms tied to synaptic plasticity and therapeutic implications. Does not specifically address Hebbian learning or nerve growth factor (NGF).

Focuses on BDNF's role in synaptic plasticity. Discusses BDNF mechanisms tied to synaptic plasticity and therapeutic implications. Does not specifically address Hebbian learning or nerve growth factor (NGF).

20.7%

5.0

2017

[53] Impaired NGF/TrkA Signaling Causes Early AD-Linked Presynaptic Dysfunction in Cholinergic Primary Neurons V. Latina, ..., and P. Calissano Frontiers in Cellular Neuroscience 2017 - 38 citations - Show abstract - Cite Abstract: Alterations in NGF/TrkA signaling have been suggested to underlie the selective degeneration of the cholinergic basal forebrain neurons occurring in vivo in AD (Counts and Mufson, 2005; Mufson et al., 2008; Niewiadomska et al., 2011) and significant reduction of cognitive decline along with an improvement of cholinergic hypofunction have been found in phase I clinical trial in humans affected from mild AD following therapeutic NGF gene therapy (Tuszynski et al., 2005, 2015). Here, we show that the chronic (10–12 D.I.V.) in vitro treatment with NGF (100 ng/ml) under conditions of low supplementation (0.2%) with the culturing serum-substitute B27 selectively enriches the basal forebrain cholinergic neurons (+36.36%) at the expense of other non-cholinergic, mainly GABAergic (−38.45%) and glutamatergic (−56.25%), populations. By taking advantage of this newly-developed septo-hippocampal neuronal cultures, our biochemical and electrophysiological investigations demonstrate that the early failure in excitatory neurotransmission following NGF withdrawal is paralleled by concomitant and progressive loss in selected presynaptic and vesicles trafficking proteins including synapsin I, SNAP-25 and α-synuclein. This rapid presynaptic dysfunction: (i) precedes the commitment to cell death and is reversible in a time-dependent manner, being suppressed by de novo external administration of NGF within 6 hr from its initial withdrawal; (ii) is specific because it is not accompanied by contextual changes in expression levels of non-synaptic proteins from other subcellular compartments; (ii) is not secondary to axonal degeneration because it is insensible to pharmacological treatment with known microtubule-stabilizing drug such paclitaxel; (iv) involves TrkA-dependent mechanisms because the effects of NGF reapplication are blocked by acute exposure to specific and cell-permeable inhibitor of its high-affinity receptor. Taken together, this study may have important clinical implications in the field of AD neurodegeneration because it: (i) provides new insights on the earliest molecular mechanisms underlying the loss of synaptic/trafficking proteins and, then, of synapes integrity which occurs in vulnerable basal forebrain population at preclinical stages of neuropathology; (ii) offers prime presynaptic-based molecular target to extend the therapeutic time-window of NGF action in the strategy of improving its neuroprotective in vivo intervention in affected patients. 20.7% topic match

20.2%

0.7

2021

[54] The Association of Brain-Derived Neurotrophic Factor with Long-Term Potentiation Z. Salimi, ..., and S. M. Ahmadi Shiraz E-Medical Journal 2021 - 2 citations - Show abstract - Cite 20.2% topic match

Reviews BDNF's role in synaptic plasticity and LTP. Examines how BDNF influences LTP through neuroprotective, synaptogenic, and synaptic transmission pathways. Does not discuss Hebbian learning specifically or the role of nerve growth factor (NGF).

Reviews BDNF's role in synaptic plasticity and LTP. Examines how BDNF influences LTP through neuroprotective, synaptogenic, and synaptic transmission pathways. Does not discuss Hebbian learning specifically or the role of nerve growth factor (NGF).

20.1%

21.6

1995

[55] Brain-derived neurotrophic factor rapidly enhances synaptic transmission in hippocampal neurons via postsynaptic tyrosine kinase receptors. E. Levine, ..., and M. Plummer Proceedings of the National Academy of Sciences of the United States of America 1995 - 630 citations - Show abstract - Cite 20.1% topic match

19.8%

0.0

2013

[56] Enhancements in mossy fibers long‐term potentiation (LTP) are neurotrophin‐specific. Esther Angelica Jimenez‐Nunez, ..., and James T. Porter The FASEB Journal 2013 - 0 citations - Show abstract - Cite 19.8% topic match

Shows specific enhancement of mossy fibers LTP by neurotrophins. Investigates the role of BDNF, NT3, and NGF in hippocampal LTP. Focuses primarily on BDNF with minimal details on NGF, relevant but not strongly aligned with NGF in Hebbian learning.

Shows specific enhancement of mossy fibers LTP by neurotrophins. Investigates the role of BDNF, NT3, and NGF in hippocampal LTP. Focuses primarily on BDNF with minimal details on NGF, relevant but not strongly aligned with NGF in Hebbian learning.

19.3%

6.0

2012

[57] MSK1 Regulates Homeostatic and Experience-Dependent Synaptic Plasticity Sonia A. L. Corrêa, ..., and B. Frenguelli The Journal of Neuroscience 2012 - 73 citations - Show abstract - Cite 19.3% topic match

Shows the role of MSK1 in synaptic plasticity. Details how BDNF initiates adaptive changes via MSK1 signaling. Does not explicitly investigate NGF or Hebbian learning mechanisms, focusing on BDNF instead.

Shows the role of MSK1 in synaptic plasticity. Details how BDNF initiates adaptive changes via MSK1 signaling. Does not explicitly investigate NGF or Hebbian learning mechanisms, focusing on BDNF instead.

19.1%

1.6

2011

[58] Neurogranin phosphorylation fine‐tunes long‐term potentiation Ling Zhong, ..., and N. Gerges European Journal of Neuroscience 2011 - 22 citations - Show abstract - Cite 19.1% topic match

18.6%

5.5

1999

[59] Gating of BDNF-induced synaptic potentiation by cAMP. L. Boulanger and M. Poo Science 1999 - 140 citations - Show abstract - Cite 18.6% topic match

Shows that cAMP modulates BDNF-induced synaptic potentiation. BDNF-induced potentiation is gated by cAMP signaling, and its effects are enhanced by cAMP activators. Does not specifically investigate Hebbian learning or involve nerve growth factor (NGF). Focuses on BDNF and cAMP pathways.

Shows that cAMP modulates BDNF-induced synaptic potentiation. BDNF-induced potentiation is gated by cAMP signaling, and its effects are enhanced by cAMP activators. Does not specifically investigate Hebbian learning or involve nerve growth factor (NGF). Focuses on BDNF and cAMP pathways.

17.7%

2.1

1998

[60] Evidence for a role for synaptophysin in expression of long‐term potentiation in rat dentate gyrus P. M. Mullany and M. Lynch NeuroReport 1998 - 55 citations - Show abstract - Cite 17.7% topic match

17.4%

10.6

2000

[61] Role of Phosphoinositide 3-Kinase and Endocytosis in Nerve Growth Factor-Induced Extracellular Signal-Regulated Kinase Activation via Ras and Rap1 Randall D. York, ..., and P. Stork Molecular and Cellular Biology 2000 - 254 citations - Show abstract - Cite 17.4% topic match

17.0%

1.5

1996

[62] trkA Mediates the Nerve Growth Factor-induced Intracellular Calcium Accumulation (*) M. D. De Bernardi, ..., and I. Mocchetti The Journal of Biological Chemistry 1996 - 42 citations - Show abstract - Cite 17.0% topic match

16.5%

33.8

1996

[63] A Requirement for Local Protein Synthesis in Neurotrophin-Induced Hippocampal Synaptic Plasticity Hyejin Kang and E. Schuman Science 1996 - 951 citations - Show abstract - Cite 16.5% topic match

Shows the requirement of local protein synthesis in neurotrophin-induced synaptic plasticity. Demonstrates that BDNF and NT-3 enhance hippocampal synaptic transmission, requiring immediate local protein synthesis. Does not mention Hebbian learning or nerve growth factor (NGF) directly, focusing instead on other neurotrophins, potentially limiting direct relevance.

Shows the requirement of local protein synthesis in neurotrophin-induced synaptic plasticity. Demonstrates that BDNF and NT-3 enhance hippocampal synaptic transmission, requiring immediate local protein synthesis. Does not mention Hebbian learning or nerve growth factor (NGF) directly, focusing instead on other neurotrophins, potentially limiting direct relevance.

15.6%

4.5

2000

[64] Brain‐derived neurotrophic factor increases activity of NR2B‐containing N‐methyl‐D‐aspartate receptors in excised patches from hippocampal neurons E. Levine and J. E. Kolb Journal of Neuroscience Research 2000 - 108 citations - Show abstract - Cite 15.6% topic match

15.6%

0.0

2009

[65] Ca2+‐sensitive redistribution of calmodulin and neurogranin in CA1 pyramidal neurons of mouse hippocampus Kuo‐ping Huang and F. Huang The FASEB Journal 2009 - 0 citations - Show abstract - Cite 15.6% topic match

15.0%

0.3

1991

[66] Nerve growth factor binds to the 140 kd trk proto-oncogene product and stimulates its association with the src homology domain of phospholipase C gamma 1. M. Ohmichi, ..., and A. Saltiel Biochemical and biophysical research communications 1991 - 11 citations - Show abstract - Cite 15.0% topic match

14.6%

5.5

1999

[67] Cytokine and Growth Factor Involvement in Long-Term Potentiation J. Jankowsky and P. Patterson Molecular and Cellular Neuroscience 1999 - 137 citations - Show abstract - Cite 14.6% topic match

13.6%

0.0

2010

[68] Long‐term potentiation (LTP) induces co‐localization of calmodulin and neurogranin in the dendritic spines of mouse hippocampal CA1 pyramidal neurons Kuo‐ping Huang and F. L The FASEB Journal 2010 - 0 citations - Show abstract - Cite 13.6% topic match

13.5%

2.1

1991

[69] The Synthesis of Nerve Growth Factor and Brain‐Derived Neurotrophic Factor in Hippocampal and Cortical Neurons Is Regulated by Specific Transmitter Systems a H. Thoenen, ..., and D. Lindholm Annals of the New York Academy of Sciences 1991 - 70 citations - Show abstract - Cite 13.5% topic match

13.0%

1.1

2003

[70] Analysis of the presynaptic signaling mechanisms underlying the inhibition of LTP in rat dentate gyrus by the tyrosine kinase inhibitor, genistein D. Pereira and C. Duarte Hippocampus 2003 - 23 citations - Show abstract - Cite 13.0% topic match

12.9%

2.0

1999

[71] Activation of TrkA by nerve growth factor upregulates expression of the cholinergic gene locus but attenuates the response to ciliary neurotrophic growth factor. B. Berse, ..., and J. Blusztajn The Biochemical journal 1999 - 50 citations - Show abstract - Cite 12.9% topic match

12.8%

4.8

2013

[72] Growth factors in synaptic function V. Y. Poon, ..., and Mikyoung Park Frontiers in Synaptic Neuroscience 2013 - 53 citations - Show abstract - Cite 12.8% topic match

Identifies neurotrophic factors involved in synaptic function. Discusses roles of netrin, Wnt, TGF-β, and TNF-α in synaptic development and plasticity. Does not directly investigate Hebbian learning or NGF involvement.

Identifies neurotrophic factors involved in synaptic function. Discusses roles of netrin, Wnt, TGF-β, and TNF-α in synaptic development and plasticity. Does not directly investigate Hebbian learning or NGF involvement.

12.5%

9.7

1994

[73] Neuronal differentiation signals are controlled by nerve growth factor receptor/Trk binding sites for SHC and PLC gamma. A. Obermeier, ..., and A. Ullrich The EMBO Journal 1994 - 296 citations - Show abstract - Cite 12.5% topic match

12.1%

0.0

2016

[74] Nerve growth factor and brain-derived neurotrophic factor attenuate angiotensin-II-induced facilitation of calcium channels in acutely dissociated nucleus tractus solitarii neurons of the rat Takayuki Endoh, ..., and M. Tazaki Journal Not Provided 2016 - 0 citations - Show abstract - Cite 12.1% topic match

11.6%

2.7

1996

[75] Determinants of BDNF-induced hippocampal synaptic plasticity: role of the Trk B receptor and the kinetics of neurotrophin delivery. Hyejin Kang, ..., and Erin M. Schuman Learning & memory 1996 - 77 citations - Show abstract - Cite 11.6% topic match

11.6%

11.2

1998

[76] Presynaptic Modulation of Synaptic Transmission and Plasticity by Brain-Derived Neurotrophic Factor in the Developing Hippocampus W. Gottschalk, ..., and B. Lu The Journal of Neuroscience 1998 - 293 citations - Show abstract - Cite Abstract: In addition to the regulation of neuronal survival and differentiation, neurotrophins may play a role in synapse development and plasticity. Application of brain-derived neurotrophic factor (BDNF) promotes long-term potentiation (LTP) in CA1 synapses of neonatal hippocampus, which otherwise exhibit only short-term potentiation. This is attributable, at least in part, to an attenuation of the synaptic fatigue induced by high-frequency stimulation (HFS). However, the prevention of synaptic fatigue by BDNF could be mediated by an attenuation of synaptic vesicle depletion from presynaptic terminals and/or a reduction of the desensitization of postsynaptic receptors. Here we provide evidence supporting a presynaptic effect of BDNF. The effect of BDNF on synaptic fatigue depended on the stimulation frequency, not on the stimulus duration nor on the number of stimulation pulses. BDNF was only effective when the synapses were stimulated at frequencies >50 Hz. Treatment with BDNF also potentiated paired-pulse facilitation (PPF), a parameter reflecting changes in the properties of presynaptic terminals. This effect of BDNF was restricted only to PPF elicited with interpulse intervals ≤20 msec. Changes in the extracellular calcium concentration altered the magnitude of the BDNF effect on PPF and synaptic responses to HFS, suggesting that BDNF regulates neurotransmitter release. When the desensitization of glutamate receptors was blocked by cyclothiazide or aniracetam, the BDNF potentiation of the synaptic responses to HFS was unaltered. Taken together, these results suggest that BDNF acts presynaptically. When two pathways in the same slice were monitored simultaneously, BDNF treatment potentiated the tetanized pathway without affecting the synaptic efficacy of the untetanized pathway. The selective potentiation of high-frequency transmission by BDNF appears to contribute directly to the effect of BDNF on LTP rather than indirectly by inducing the release of additional diffusible factors. The preferential potentiation of highly active synapses by BDNF may have implications in the Hebbian mechanism of synaptic plasticity. 11.6% topic match

11.4%

44.0

2003

[77] BDNF and activity-dependent synaptic modulation. B. Lu Learning & memory 2003 - 952 citations - Show abstract - Cite 11.4% topic match

11.3%

1.5

1993

[78] Monocular deprivation effects in the rat visual cortex and lateral geniculate nucleus are prevented by nerve growth factor (NGF). I. Visual cortex N. Berardi, ..., and L. Maffei Proceedings of the Royal Society of London. Series B: Biological Sciences 1993 - 47 citations - Show abstract - Cite 11.3% topic match

Shows that NGF prevents effects of monocular deprivation in rat visual cortex. Demonstrates that NGF treatment maintains ocular dominance distribution and visual acuity by preventing monocular deprivation-induced changes. Does not directly address the molecular mechanisms of Hebbian learning or NGF in synaptic plasticity; focus on visual cortex plasticity.

Shows that NGF prevents effects of monocular deprivation in rat visual cortex. Demonstrates that NGF treatment maintains ocular dominance distribution and visual acuity by preventing monocular deprivation-induced changes. Does not directly address the molecular mechanisms of Hebbian learning or NGF in synaptic plasticity; focus on visual cortex plasticity.

10.8%

1.3

2005

[79] Nerve Growth Factor Rapidly Increases Muscarinic Tone in Mouse Medial Septum/Diagonal Band of Broca C. K. Wu and H. Yeh The Journal of Neuroscience 2005 - 26 citations - Show abstract - Cite 10.8% topic match

10.7%

1.1

1999

[80] Voltage-sensitive calcium currents are acutely increased by nerve growth factor in PC12 cells. M. Jia, ..., and G. Guroff Journal of neurophysiology 1999 - 27 citations - Show abstract - Cite 10.7% topic match

10.6%

2.7

2020

[81] Neurogranin Regulates Metaplasticity Ling Zhong and N. Gerges Frontiers in Molecular Neuroscience 2020 - 13 citations - Show abstract - Cite 10.6% topic match

10.5%

0.5

1997

[82] Activation of calcium-dependent potassium channels in mouse [correction of rat] brain neurons by neurotrophin-3 and nerve growth factor. N. R. Holm, ..., and S. Gammeltoft Proceedings of the National Academy of Sciences of the United States of America 1997 - 14 citations - Show abstract - Cite 10.5% topic match

10.3%

1.0

2000

[83] Intracellular Ca(2+) signaling is required for neurotrophin-induced potentiation in the adult rat hippocampus. H. Kang and E. Schuman Neuroscience letters 2000 - 25 citations - Show abstract - Cite 10.3% topic match

10.0%

4.1

2000

[84] Brain-Derived Neurotrophic Factor Acutely Inhibits AMPA-Mediated Currents in Developing Sensory Relay Neurons A. Balkowiec, ..., and D. Katz The Journal of Neuroscience 2000 - 102 citations - Show abstract - Cite 10.0% topic match

10.0%

0.3

1998

[85] Partial cortical devascularization results in elevations of cortical nerve growth factor and increases nerve growth factor protein within basal forebrain cholinergic neurons J. Conner, ..., and S. Varon Neuroscience 1998 - 7 citations - Show abstract - Cite 10.0% topic match

9.9%

17.8

1994

[86] Neurotrophin signal transduction by the Trk receptor. D. Kaplan and R. Stephens Journal of neurobiology 1994 - 535 citations - Show abstract - Cite 9.9% topic match

9.8%

0.4

2002

[87] Analysis of the presynaptic signaling mechanisms underlying the inhibition of LTP in rat dentate gyrus by the tyrosine kinase inhibitor, genistein M. Casey, ..., and M. Lynch Hippocampus 2002 - 10 citations - Show abstract - Cite 9.8% topic match

9.7%

0.0

2000

[88] Selective Potentiation at Excitatory Synapses No author found Science's STKE 2000 - 0 citations - Show abstract - Cite 9.7% topic match

9.3%

10.0

1994

[89] Positive Feedback between Acetylcholine and the Neurotrophins Nerve Growth Factor and Brain‐derived Neurotrophic Factor in the Rat Hippocampus M. Knipper, ..., and D. Lindholm European Journal of Neuroscience 1994 - 307 citations - Show abstract - Cite 9.3% topic match

9.2%

0.1

2015

[90] Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function Akira Yoshii, ..., and N. Ip Frontiers in Synaptic Neuroscience 2015 - 1 citations - Show abstract - Cite 9.2% topic match

9.1%

16.6

1998

[91] Brain-derived neurotrophic factor modulates hippocampal synaptic transmission by increasing N-methyl-D-aspartic acid receptor activity. E. Levine, ..., and M. Plummer Proceedings of the National Academy of Sciences of the United States of America 1998 - 434 citations - Show abstract - Cite 9.1% topic match

9.0%

34.1

2002

[92] Brain-Derived Neurotrophic Factor Induces Long-Term Potentiation in Intact Adult Hippocampus: Requirement for ERK Activation Coupled to CREB and Upregulation of Arc Synthesis S. Ying, ..., and C. Bramham The Journal of Neuroscience 2002 - 772 citations - Show abstract - Cite 9.0% topic match

8.6%

0.0

2004

[93] Trking Down an Inside Job No author found Science's STKE 2004 - 0 citations - Show abstract - Cite Abstract: Nerve growth factor (NGF) binds to the TrkA receptor tyrosine kinase at the cell surface, leading to receptor autophosphorylation and activation of intracellular signaling pathways. However, ligand binding to some G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptors (GPCRs), such as the adenosine A2A receptor or the pituitary adenylate cyclase-activating polypeptide (PACAP) PAC1 receptor, can independently stimulate TrkA phosphorylation and activation of TrkA signaling pathways. Rajagopal et al. used phosphotyrosine-specific antibodies on pan-Trk immunoprecipitates of PC12-615 cells to investigate TrkA phosphorylation in response to adenosine and observed that forms of the TrkA receptor that are not targeted to the plasma membrane were phosphorylated first. Inhibitors of transcription or translation blocked phosphorylation in response to the adenosine agonist CGS 21680 but not phosphorylation induced by NGF; reverse transcription polymerase chain reaction (RT-PCR) indicated that CGS 21680 treatment did not elicit NGF production. Cell surface biotinylation experiments indicated that CGS 21680 activated an intracellular pool of Trk receptors. Immunofluorescence analysis in combination with confocal microscopy revealed that, whereas NGF treatment stimulated TrkA phosphorylation at the plasma membrane, CGS 21680 activated perinuclear TrkA associated with the Golgi apparatus. Moreover, pharmacological inhibition of Golgi vesicle fusion abolished perinuclear TrkA immunoreactivity and blocked CGS 21680-dependent TrkA phosphorylation and the downstream phosphorylation of Akt. PACAP stimulated a similar pattern of perinuclear immunofluorescence in primary cultures of basal forebrain neurons. Thus, GPCR-dependent activation of TrkA appears to take place in an intracellular compartment, a finding the authors discuss in the context of retrograde signaling from internalized TrkA receptors. R. Rajagopal, Z.-Y. Chen, F. S. Lee, M. V. Chao, Transactivation of Trk neurotrophin receptors by G-protein-coupled receptor ligands occurs on intracellular membranes. J. Neurosci. 24, 6650-6658 (2004). [Abstract] [Full Text] 8.6% topic match

8.5%

1.2

1997

[94] Expression of human p140trk receptors in p140trk‐deficient, PC12/endothelial cells results in nerve growth factor‐induced signal transduction and DNA synthesis Hao Jiang, ..., and P. Lazarovici Journal of Cellular Biochemistry 1997 - 32 citations - Show abstract - Cite Abstract: Nerve growth factor (NGF) regulates proliferation, differentiation, and survival of sympathetic and sensory neurons through the tyrosine kinase activity of its receptor, p140trk. These biological effects of NGF depend upon the signal‐mediating function of p140trk substrates which are likely to differ from cell to cell. To define p140trk receptor substrates and the details of signalling by NGF in the hybrid cell PC12EN, we stably transfected cultures with a vector encoding a full‐length human p140trk cDNA sequence. Two stably transfected clones, one expressing p140trk with higher affinity (PC12EN‐trk3; Kd 57.4 pM, Bmax 9.7 pmole/mg) and one expressing p140trk with a lower affinity (PC12EN‐trk1; Kd 392.4 pM, Bmax 5.7 pmole/mg) were generated. Radioreceptor assays indicate that transfected p140trk receptors show slow NGF‐dissociation kinetics, are resistant to trypsin or Triton X‐100 treatment, are specific for NGF compared to other neurotrophins, and are internalized or downregulated as are native PC12 p140trk receptors. NGF stimulates p140trk tyrosine phosphorylation in a dose‐ (0.01‐10 ng/ml) and time‐ (5‐120 min) dependent manner, and tyrosine phosphorylation was inhibited by 200‐1,000 nM K‐252a. NGF‐induced Erk stimulation for 60 min was assessed using myelin basic protein as a substrate. NGF treatment also led to an increased phosphorylation of p70S6k, SNT, and phospholipase Cγ, demonstrating that the major NGF‐stimulated signalling pathways found in other cells are activated in PC12EN‐trk cells. Staurosporine (5‐50 nM) rapidly and dBcAMP (1 mM) more slowly, but not NGF induced morphological differentiation in PC12EN‐trk cells. Rather, NGF treatment in low‐serum medium stimulated a 1.3‐ and 2.3‐fold increase in DNA synthesis measured by [3H]thymidine incorporation in PC12EN‐trk1 and PC12EN‐trk3, respectively. These data highlight the functionality of the transfected p140trk receptors and indicate that these transfected cells may serve as a novel cellular model facilitating the study of the mitogenic properties of NGF signalling and the transducing role of the p140trk receptor substrates. J. Cell. Biochem. 66:229‐244. © 1997 Wiley‐Liss, Inc. This article is a U.S. Government work and, as such, is in the public domain in the United States of America. 8.5% topic match

8.4%

None

[95] Nerve growth factor prevents the amblyopic effects of monocular deprivation ( visual plasticity / neurotrophic factors / rat L. Domenici, ..., and L. Maffei Journal Not Provided None - 1 citations - Show abstract - Cite Abstract: Monocular deprivation early in life causes dramatic changes in the functional organization ofmammalian visual cortex and severe reduction in visual acuity and contrast sensitivity of the deprived eye. We tested whether or not these changes could be from competition between the afferents from the two eyes for a target-derived neurotrophic factor. Rats monocularly deprived during early postnatal development were treated with repetitive intraventricular injections or topical administration of nerve growth factor. The effects of monocular deprivation were then assessed electrophysiologically. In untreated animals visual acuity and contrast sensitivity of the deprived eye were strongly reduced, whereas in nerve growth factor-treated animals these parameters were normal. Manipulations of the visual environment during early postnatal life (critical period) of mammals lead to dramatic changes in organization of the visual cortex. For example, monocular deprivation by temporary closure of one eye renders neurons in the striate cortex largely unresponsive to visual stimulation of the deprived eye, shifting oculardominance distribution in favor of the nondeprived eye (1-3). The deprived eye becomes amblyopic-i.e., visual acuity is dramatically impaired, and contrast sensitivity is depressed (4-6). The effects of monocular deprivation have usually been ascribed to competition between the two monocular inputs to binocular cortical neurons. Since this binocular-competition hypothesis was proposed by Wiesel and Hubel (1), several factors have been shown to prevent the plastic changes induced in visual cortex by monocular deprivation during the critical period (7-11). However, no one has sought to determine for what the afferents from the two eyes might be competing during early development. We propose the hypothesis that this competition between afferents is for a neurotrophic factor, the production ofwhich is activity dependent. The activity in afferents from the deprived eye could be insufficient or inappropriate for the necessary production (or uptake) of neurotrophic factor, leading to decreased synaptic efficacy of these afferents. To test this hypothesis we assessed whether an exogenous supply of nerve growth factor (NGF) (13) could prevent the effects of monocular deprivation on the ocular-dominance distribution, visual acuity, and contrast sensitivity of the deprived eye in rats during the critical period (12). Our data show that NGF, given exogenously, preserves visual acuity and contrast sensitivity of the deprived eye. That NGF also prevents the change in ocular-dominance distribution has been reported (14). MATERIALS AND METHODS A total of 59 Long-Evans hooded rats were used in these experiments: 40 rats for visual evoked potentials (VEP) and cell recordings, 4 rats for the estimation of NGF diffusion, and 15 rats for determination of choline acetyltransferase (ChoAcT) activity. VEP and Cell Recordings. Animal treatment. We used 11 normal and 29 monocularly deprived rats. Rats were monocularly deprived for 1 mo by suturing one eyelid from postnatal day 14 (P14; time of natural eye opening) to P45. This procedure effectively spans the whole length of the critical period in rat (12). Ten rats were only monocularly deprived. Thirteen rats were monocularly deprived and repetitively injected (2 Al) into the lateral ventricle with B-NGF (1-1.6 ,tg/1xl)/buffered saline (nine rats), with cytochrome c (1 ,4g/,41)/buffered saline (two rats), or with vehicle alone (two rats). Rats were injected every other day for 1 mo through a microsyringe connected with a cannula (26 gauge) inserted through a skull hole 1 mm lateral and in correspondence with bregma, entering the lateral ventricle (15). When dye (Pontamine sky blue) was injected by this procedure, it was invariably found in the ventricles. In the other six rats, monocular deprivation was combined with local application to the visual cortex of one hemisphere of a small (=-1 mm2) piece of fibrine (Zimospuma, 80% fibrine/20% NaCl, Baldacci Laboratories, Pisa, Italy) placed 1 mm anterior with respect to the visual cortex. Fibrine was soaked with 2 pLI of either NGF at 1.6 ug/IL/buffered saline (four rats) or vehicle alone (two rats). Treatments were repeated every 2 days for 2 weeks by injecting, through a microcannula, 1 pA of the appropriate solution into the fibrine patch. After 1 week the old patch was replaced with another one. In these rats monocular deprivation was continued for only 2 weeks. Eyelid suture, injections, and topical applications were done under chloral hydrate anesthesia (0.4 g/kg i.p.). Recordings. Of the 11 normal rats, recordings were made of four rats after P45, of two rats at P19, of two rats at P21, and of three rats at P30. All monocularly deprived rats were tested at the end of the deprivation period (1 mo for intraventricular treatment and 2 weeks for local treatment). Recordings were made in urethane-anesthetized rats (1200 mg/kg i.p.). VEP evoked by different visual stimuli to either eye were recorded by inserting a micropipette, filled with 3 M NaCl, into the binocular portion of either visual cortex (binocular area 17 or area OC1B). Eyes of the animals were fixed by means of metal rings. Correct location of the micropipette was checked by recording single-unit activity at the beginning of the experimental session and ascertaining that (i) the cell receptive fields were in the central portion of Abbreviations: NGF, nerve growth factor; VEP, visual evoked potentials; ChoAcT, choline acetyltransferase; Pn, postnatal day n. tTo whom reprint requests should be addressed. 8811 The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. 8812 Neurobiology: Domenici et al. the visual field (within 200 from the vertical meridian) and in the upper quadrant and (it) binocular units could be recorded. In three rats recordings were also made in the monocular portion of the visual cortex (monocular area 17 or area OCiM), as judged by location of the cell receptive fields and ocular dominance. The visual stimuli were vertical gratings of different spatial frequencies generated on a display (HP Hewlett-Packard model 1300 A, mean luminance 12 cycles / in2) positioned 20 cm from the rat eyes and centered on the previously determined receptive fields. The gratings were alternated in phase with a fixed temporal frequency, from the 2-4 Hz range. The signals were filtered and amplified in a conventional manner, computer-averaged, and analyzed. For each condition (visual cortex, viewing eye, spatial frequency, contrast) at least 400 responses were averaged. For each record the amplitude, phase, and relative power of the first 12 harmonics were measured. For the temporal frequencies used, signals consisted mainly of the second harmonic (relative power >70%). For this reason, amplitude of the second harmonic in each record (1/2 peak-to-trough amplitude) was taken as the VEP amplitude for that condition. Noise level for a given condition (temporal frequency of alternation, viewing eye, visual cortex) was considered to be the amplitude of the second harmonic in records where the stimulus was covered with a translucent screen. To assess the spatial resolution value (visual acuity), gratings of maximum available contrast were used (70%6); spatial frequency was progressively increased until signal was indistinguishable from noise. Visual acuity was measured as the highest spatial frequency that still evoked a response above noise level. To test whether animals needed any optical correction, recordings were made with and without lenses of different dioptric power placed before the rat eyes. The lens that imparted highest visual acuity was considered optimal. The contrast threshold at a given spatial frequency was evaluated by extrapolating to zero voltage (noise level) the linear regression through a contrast response curve (VEP amplitude vs. logarithm of stimulus contrast) (16, 17). Contrast sensitivity is the reciprocal of contrast threshold. Determination of ChoAcT Activity. Fifteen rats were used, all monocularly deprived at P14 and treated intraventricularly with either NGF (n = 10) or cytochrome c (n = 5) under the above-mentioned protocols. These rats were sacrificed at P45 by cervical dislocation. Brains were rapidly removed, and the occipital cortices were dissected on ice and stored at -800C until assayed. ChoAcT activity was determined by described procedures (18, 19) with minor modifications. Enzyme activity was expressed on the basis of protein content (20). Diffusion of NGF. To estimate diffusion ofNGF, a piece of fibrine loaded with 1 lI (0.08 ,ACi; 1 Ci = 37 GBq) of 125I-labeled NGF (specific activity 72.2 ,Ci/jtg) was applied to the cortical surface (anterior-posterior bregma, left 2 mm) in four rats. The animals were sacrificed 24 hr later, and the whole brains were dissected and frozen. Serial transverse sections of the neocortex 1 mm thick were cut from the injection site in a rostrocaudal direction. The radioactivity in the sections was counted by a y counter (model Cobra, Hewlett-Packard). Table 1. Visual acuities in monocularly deprived and monocularly deprived NGF-treated rats Visual acuity, cycles/degree Nondeprived eye Deprived eye Animal Treatment Ipsi Contra Ipsi Contra Depl MD 1.0 1.1 0.45 0.35 Dep2 MD 1.0 0.35 Dep3t MD 1.1 1.0 0.25 0.5 Dep4 MD 1.0 1.0 0.45 0.5 Dep5t MD 1.1 0.3 0.5 Dep6 MD 1.1 1.05 0.3 Dep7 MD 0.9 1.0 0.3 0.35 8.4% topic match

8.2%

0.0

2008

[96] TRPC Channels as Novel Effectors of BDNF Signaling: Potential Implications for Rett Syndrome M. Amaral, ..., and Lucas Pozzo-Miller Journal Not Provided 2008 - 0 citations - Show abstract - Cite 8.2% topic match

8.2%

14.7

2005

[97] The p75 Neurotrophin Receptor Negatively Modulates Dendrite Complexity and Spine Density in Hippocampal Neurons M. Zagrebelsky, ..., and M. Korte The Journal of Neuroscience 2005 - 280 citations - Show abstract - Cite 8.2% topic match

8.2%

2.2

2019

[98] A kinetic model for Brain-Derived Neurotrophic Factor mediated spike timing-dependent LTP S. Solinas, ..., and M. Migliore PLoS Computational Biology 2019 - 12 citations - Show abstract - Cite Abstract: Across the mammalian nervous system, neurotrophins control synaptic plasticity, neuromodulation, and neuronal growth. The neurotrophin Brain-Derived Neurotrophic Factor (BDNF) is known to promote structural and functional synaptic plasticity in the hippocampus, the cerebral cortex, and many other brain areas. In recent years, a wealth of data has been accumulated revealing the paramount importance of BDNF for neuronal function. BDNF signaling gives rise to multiple complex signaling pathways that mediate neuronal survival and differentiation during development, and formation of new memories. These different roles of BDNF for neuronal function have essential consequences if BDNF signaling in the brain is reduced. Thus, BDNF knock-out mice or mice that are deficient in BDNF receptor signaling via TrkB and p75 receptors show deficits in neuronal development, synaptic plasticity, and memory formation. Accordingly, BDNF signaling dysfunctions are associated with many neurological and neurodegenerative conditions including Alzheimer’s and Huntington’s disease. However, despite the widespread implications of BDNF-dependent signaling in synaptic plasticity in healthy and pathological conditions, the interplay of the involved different biochemical pathways at the synaptic level remained mostly unknown. In this paper, we investigated the role of BDNF/TrkB signaling in spike-timing dependent plasticity (STDP) in rodent hippocampus CA1 pyramidal cells, by implementing the first subcellular model of BDNF regulated, spike timing-dependent long-term potentiation (t-LTP). The model is based on previously published experimental findings on STDP and accounts for the observed magnitude, time course, stimulation pattern and BDNF-dependence of t-LTP. It allows interpreting the main experimental findings concerning specific biomolecular processes, and it can be expanded to take into account more detailed biochemical reactions. The results point out a few predictions on how to enhance LTP induction in such a way to rescue or improve cognitive functions under pathological conditions. 8.2% topic match

8.0%

4.3

2007

[99] NGF-cholinergic dependency in brain aging, MCI and Alzheimer's disease. A. Cuello, ..., and K. Bell Current Alzheimer research 2007 - 74 citations - Show abstract - Cite Abstract: Forebrain cholinergic neurons are highly dependent on nerve growth factor (NGF) for phenotype maintenance. We have established that in addition to "target-derived" NGF neurotrophic stimulation, cholinergic neurons also respond dose-dependently, to intra-parenchymal NGF administration in the somato-dendritic region of the nucleus Basalis, thus illustrating the potential of alternative reparative therapies which would by-pass the undesirable effects of diffuse neurotrophin application. Moreover, our lab has also observed that the steady-state number of cortical cholinergic synapses is dependent on continuous NGF supply, as anti-NGF monoclonal antibodies and TrkA receptor antagonists deplete pre-existing cholinergic bouton numbers. Furthermore, the application of either NGF or TrkA NGF-mimetic agonists successfully rescues the age-dependent loss of cortical cholinergic boutons in aged-impaired rats. The vulnerability of the cortical cholinergic system has also been demonstrated in transgenic animal models of the Alzheimer's disease (AD) amyloid pathology. It is of interest to note however, that an up-regulation of cholinergic presynaptic boutons has been observed in certain transgenic mouse models prior to plaque formation. This observation is similar to the visibly increased immunoreactivity of cortical and hippocampal choline acetyltransferase (ChAT) fibers in patients with Mild Cognitive Impairment (MCI). A series of ex-vivo experiments conducted by our group have demonstrated that contrary to popular belief, proNGF, as opposed to mature NGF, is released from the cerebral cortex in an activity-dependent manner. In addition, proNGF appears to be released with a series of pro-enzymes and enzymes, which are involved in its subsequent maturation to NGF and degradation in the extracellular space. Given that proNGF is known to be upregulated in AD patients a dysregulation in the maturation or degradation of mature NGF might explain the preferential vulnerability of the cholinergic system in the AD pathology. 8.0% topic match

7.9%

2.5

2005

[100] Gene Expression in the Conversion of Early‐Phase to Late‐Phase Long‐Term Potentiation Philip R. Lee, ..., and R. Fields Annals of the New York Academy of Sciences 2005 - 49 citations - Show abstract - Cite 7.9% topic match

7.7%

10.9

1999

[101] Neurotrophins and hippocampal synaptic transmission and plasticity B. Lu and A. Chow Journal of Neuroscience Research 1999 - 272 citations - Show abstract - Cite 7.7% topic match

7.7%

1.4

1998

[102] NGF induces transient but not sustained activation of ERK in PC12 mutant cells incapable of differentiating R. Yaka, ..., and R. Stein Journal of Cellular Biochemistry 1998 - 36 citations - Show abstract - Cite 7.7% topic match

7.7%

1.2

2000

[103] Nerve growth factor activation of the extracellular signal-regulated kinase pathway is modulated by Ca(2+) and calmodulin. J. Egea, ..., and J. Comella Molecular and cellular biology 2000 - 29 citations - Show abstract - Cite 7.7% topic match

7.6%

57.7

1999

[104] Neurotrophins and synaptic plasticity. A. McAllister, ..., and D. Lo Annual review of neuroscience 1999 - 1489 citations - Show abstract - Cite 7.6% topic match

7.4%

13.2

2004

[105] Induction of long-term potentiation and depression is reflected by corresponding changes in secretion of endogenous brain-derived neurotrophic factor. G. Aicardi, ..., and M. Canossa Proceedings of the National Academy of Sciences of the United States of America 2004 - 263 citations - Show abstract - Cite 7.4% topic match

7.3%

3.2

2020

[106] Neurogranin stimulates Ca2+/calmodulin-dependent kinase II by suppressing calcineurin activity at specific calcium spike frequencies Lu Li, ..., and S. Edelstein PLoS Computational Biology 2020 - 15 citations - Show abstract - Cite 7.3% topic match

7.2%

3.1

1995

[107] Differential Regulation of p21ras Activation in Neurons by Nerve Growth Factor and Brain-derived Neurotrophic Factor (*) B. Carter, ..., and Y. Barde The Journal of Biological Chemistry 1995 - 89 citations - Show abstract - Cite 7.2% topic match

7.1%

6.1

2009

[108] A Simple Role for BDNF in Learning and Memory? Carla Cunha, ..., and Kerrie L. Thomas Frontiers in Molecular Neuroscience 2009 - 91 citations - Show abstract - Cite 7.1% topic match

7.0%

6.5

2008

[109] Presynaptic and postsynaptic NMDA receptors mediate distinct effects of brain-derived neurotrophic factor on synaptic transmission. Joseph c. Madara and E. Levine Journal of neurophysiology 2008 - 103 citations - Show abstract - Cite 7.0% topic match

7.0%

7.8

2006

[110] Identification of genes co‐upregulated with Arc during BDNF‐induced long‐term potentiation in adult rat dentate gyrus in vivo K. Wibrand, ..., and C. Bramham European Journal of Neuroscience 2006 - 145 citations - Show abstract - Cite 7.0% topic match

7.0%

7.6

1999

[111] Trophic regulation of synaptic plasticity. I. Black Journal of neurobiology 1999 - 191 citations - Show abstract - Cite 7.0% topic match

6.9%

3.3

1991

[112] Nerve growth factor prevents the amblyopic effects of monocular deprivation. L. Domenici, ..., and L. Maffei Proceedings of the National Academy of Sciences of the United States of America 1991 - 109 citations - Show abstract - Cite 6.9% topic match

6.9%

3.1

2004

[113] Nerve growth factor, brain‐derived neurotrophic factor, and neurotrophin‐3 are sorted to dense‐core vesicles and released via the regulated pathway in primary rat cortical neurons Y. Wu, ..., and J. Cosgaya Journal of Neuroscience Research 2004 - 64 citations - Show abstract - Cite 6.9% topic match

6.8%

7.5

2009

[114] Nerve Growth Factor as a Signaling Molecule for Nerve Cells and also for the Neuroendocrine-Immune Systems M. Fiore, ..., and L. Aloe Reviews in the Neurosciences 2009 - 119 citations - Show abstract - Cite 6.8% topic match

6.8%

0.0

2010

[115] The nerve growth factor receptor TrkA exists as a pre‐formed homodimer before ligand binding Jian-ying Shen and I. Maruyama The FASEB Journal 2010 - 0 citations - Show abstract - Cite 6.8% topic match

6.7%

1.1

2005

[116] Multiple acute effects on the membrane potential of PC12 cells produced by nerve growth factor (NGF) K. Shimazu, ..., and G. Guroff Journal of Cellular Physiology 2005 - 21 citations - Show abstract - Cite 6.7% topic match

6.7%

2.9

2013

[117] Plasticity and metaplasticity of adult rat hippocampal mossy fibers induced by neurotrophin‐3 L. Ramos-Languren and M. Escobar European Journal of Neuroscience 2013 - 33 citations - Show abstract - Cite 6.7% topic match

6.7%

19.7

1995

[118] Inhibition of ocular dominance column formation by infusion of NT-4/5 or BDNF R. Cabelli, ..., and C. Shatz Science 1995 - 582 citations - Show abstract - Cite 6.7% topic match

6.7%

2.5

1996

[119] Basic Fibroblast Growth Factor Increases Functional L-Type Ca2+ Channels in Fetal Rat Hippocampal Neurons: Implications for Neurite Morphogenesis In Vitro Yoshitsugu Shitaka, ..., and H. Katsuki The Journal of Neuroscience 1996 - 69 citations - Show abstract - Cite 6.7% topic match

6.6%

8.8

2002

[120] Neurotrophin secretion from hippocampal neurons evoked by long-term-potentiation-inducing electrical stimulation patterns A. Gärtner and V. Staiger Proceedings of the National Academy of Sciences of the United States of America 2002 - 197 citations - Show abstract - Cite 6.6% topic match

6.6%

0.2

2004

[121] Analysis of the presynaptic signalling mechanisms underlying the inhibition of LTP in rat dentate gyrus by the tyrosine kinase inhibitor, genistein M. Lynch Hippocampus 2004 - 5 citations - Show abstract - Cite 6.6% topic match

6.6%

4.5

2000

[122] Localization of brain‐derived neurotrophic factor and trkb receptors to postsynaptic densities of adult rat cerebral cortex C. Aoki, ..., and I. Black Journal of Neuroscience Research 2000 - 111 citations - Show abstract - Cite Abstract: Although neurotrophins are critical for neuronal survival and differentiation, recent studies suggest that they also regulate synaptic plasticity. Brain‐derived neurotrophic factor (BDNF) rapidly increases synaptic transmission in hippocampal neurons, and enhances long‐term potentiation (LTP), a cellular and molecular model of learning and memory. Loci and precise mechanisms of BDNF action remain to be defined: evidence supports both pre‐ and postsynaptic sites of action. To help elucidate the synaptic mechanisms of BDNF action, we used antisera directed against the extracellular and intracellular domains of trkB receptors, anti‐trkBout and anti‐trkBin, respectively, to localize the receptors in relation to synapses. Synaptic localization of BDNF was examined in parallel using anti‐BDNF antisera. By light microscopy, trkBin and trkBout immunoreactivities were localized to hippocampal neurons and all layers of the overlying visual cortex. Immunoelectron microscopic analysis of the cerebral cortex revealed that trkB and BDNF localize discretely to postsynaptic densities (PSD) of axo‐spinous asymmetric synaptic junctions, that are the morphological correlates of excitatory, glutamatergic synapses. TrkB immunoreactivity was also detected in the nucleoplasm by light and electron microscopy. Western blot analysis indicated that both anti‐trkBout and anti‐trkBin antisera react with a protein band in the PSD corresponding to the molecular weight expected for trkB; however, molecular species distinct from that for trkB were recognized in the nuclear fraction by both anti‐trkBin and anti‐trkBout antisera, indicating that the nuclear immunoreactivity, seen by immunocytochemistry, reflects cross‐reactivity with proteins closely related to, but distinct from, trkB. The PSD localization of both BDNF and trkB supports the contention that this receptor/ligand pair participates in postsynaptic plasticity. J. Neurosci. Res. 59:454–463, 2000 © 2000 Wiley‐Liss, Inc. 6.6% topic match

6.5%

1.5

2002

[123] Expression of the Nerve Growth Factor Receptors TrkA and p75NTR in the Visual Cortex of the Rat: Development and Regulation by the Cholinergic Input F. M. Rossi, ..., and L. Maffei The Journal of Neuroscience 2002 - 35 citations - Show abstract - Cite 6.5% topic match

6.5%

0.0

2005

[124] Enhancement of synaptic transmission induced by BDNF in cultured cortical neurons Jun He, ..., and Qingming Luo https://doi.org/10.1117/12.592072 2005 - 0 citations - Show abstract - Cite 6.5% topic match

6.4%

1.9

1994

[125] NOS induction by NGF in basal forebrain cholinergic neurones: evidence for regulation of brain NOS by a neurotrophin D. Holtzman, ..., and W. Mobley Neurobiology of Disease 1994 - 56 citations - Show abstract - Cite 6.4% topic match

6.4%

0.0

1999

[126] Cytokine and growth factor involvement in long-term potentiation. J. Jankowsky and P. Patterson Molecular and cellular neurosciences 1999 - 0 citations - Show abstract - Cite 6.4% topic match

6.4%

0.5

2001

[127] Restoration of decreased N-methyl-d-asparate receptor activity by brain-derived neurotrophic factor in the cultured hippocampal neurons: involvement of cAMP. J. Sun, ..., and C. A. Wang Archives of biochemistry and biophysics 2001 - 11 citations - Show abstract - Cite 6.4% topic match

6.3%

0.9

1987

[128] Nerve growth factor is a neurotrophic factor for forebrain cholinergic neurons; implications for Alzheimer's disease. F. Hefti and B. Will Journal of neural transmission. Supplementum 1987 - 34 citations - Show abstract - Cite 6.3% topic match

6.3%

None

[129] Expression of the Nerve Growth Factor Receptors Trka and P75 Ntr in the Visual Cortex of the Rat: Development and Regulation by the Cholinergic Input Francesco Mattia Rossi, ..., and L. Maffei Journal Not Provided None - 4 citations - Show abstract - Cite Abstract: Several lines of evidence have shown that nerve growth factor (NGF), the progenitor of the neurotrophin family of growth factors, plays a fundamental role in the developmental plasticity of the rat visual cortex. However, the expression of NGF receptors (NGFRs) TrkA and p75 NTR and the possible sites of NGF action in the visual cortex remain to be elucidated so far. Using a highly sensitive ECL immunoblot analysis, we have been able to show, in the present study, that the TrkA protein is expressed in the rat visual cortex and that it is developmentally upregu-lated during the critical period for cortical plasticity. In contrast, the expression level of the low-affinity NGF receptor p75 NTR seems to remain nearly constant throughout development. In the analysis of possible pathways involved in the regulation of NGFR expression, we found that neither blockade of the visual input nor NGF administration to the visual cortex resulted in a modulation of NGFR levels of expression. On the other hand, the selective destruction of cholinergic afferents to the visual cortex caused a dramatic, but not complete, reduction of the cortical NGFRs, which suggests that these receptors are located on cholinergic terminals predominantly. At the functional level, we found that, after the elimination of the cholinergic afferents to the visual cortex, the NGF-induced increase of both acetylcholine and glutamate release from cortical synapto-somes was strongly impaired. These results indicate that the cholinergic input is an important mediator of visual cortex responsiveness to NGF action. The neurotrophins of the nerve growth factor (NGF) family, including brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4), are important modulators of the developmental plasticity in the mammalian Neurotrophins act through binding to membrane receptors belonging to the tyrosine kinase family, Trks. NGF binds TrkA, BDNF and NT-4 bind TrkB, and NT-3 binds TrkC. The interaction with Trks induces dimeriza-tion, autophosphorylation of the receptors, and successive activation of different signal transduction pathways (Bothwell, 1995; Chao and Hempstead, 1995). Moreover, all neurotrophins bind with a lower-affinity p75 N TR , a member of the tumor necrosis factor family of receptors. p75 N TR can modify the binding and function of neurotrophins when coexpressed with Trks. In the absence of Trks, NGF activation of p75 N TR may induce a cell death program, a distinct property of p75 Several lines of evidence have demonstrated the prominent role of NGF in the plasticity of the visual … 6.3% topic match

6.1%

6.8

2006

[130] Hippocampal Long-Term Potentiation Is Supported by Presynaptic and Postsynaptic Tyrosine Receptor Kinase B-Mediated Phospholipase Cγ Signaling A. Gärtner, ..., and M. Korte The Journal of Neuroscience 2006 - 127 citations - Show abstract - Cite 6.1% topic match

6.1%

None

[131] Nerve growth factor-induced ocular dominance plasticity in adult cat visual cortex ( neurotrophic factor / striate cortex / monocular deprivation ) Q. Gu, ..., and M. Cynader Journal Not Provided None - 0 citations - Show abstract - Cite Abstract: Activity-dependent modifiability of cortical ocular dominanc occurs only during early postnatal life, within the so-called "critical period," but not thereafter in adult visual cortex. To examine the role of neurotrophins in the activityand age-dependent imulation-induced moifib of visual cortex, we tested whether intracortical inion of nerve growth factor could induce ocular dominance plasticity in adult visual cortex. Nerve growth factor was continuously infused, by means of osmotic minipumps, into striate cortex of adult cats for 2 weeks. At the time of minipump implantation, one eyelid of the experimental animals was sutured closed. After 3 weeks of monocular deprivation, the ocular dominance distribution of neurons in the striate cortex was a sd uing single unit recording. We found that monocular deprivation imposed on adult animals in conjunction with nerve growth factor infusion causes an ocular dominance shift toward the deprived eye. Although the underlying mechanisms remain uncertain, the results indicate that nerve growth factor can enhance activity-dependent synaptic modification and remodeling in adult visual cortex. Over 30 years ago Wiesel and Hubel (1) showed that depriving one eye of visual input during early postnatal development caused that eye to lose functional connections with the visual cortex and to lose visual capabilities as well. Since then, intense investigations of this ocular dominance (OD) plasticity have identified neuronal activity (2), several neurotransmitters (3-5) and receptors (6-10), as well as hormones (11) and growth factors (12-14) as being involved in this process. Normally, cortical OD plasticity occurs only within a transient "critical period" during early postnatal development, but not thereafter in adult animals (15-17). To examine the hypothesis that intracortical infusion of nerve growth factor (NGF) may enhance functional modifications in mature visual cortex, we studied OD plasticity in adult cat visual cortex treated with NGF. We report here that monocular deprivation imposed on adult animals causes anOD shift toward the deprived eye. The results show that substantial synaptic modification can be reinstated even in the mature visual cortex. MATERIALS AND METHODS A total of 12 adult cats was used in this study. They were between 2 and 3 years of age, long after the end of the critical period (15-17). The monocular eyelid suture and osmotic minipump implantation were performed in the same surgical intervention under i.v. Brietal (methohexital sodium) anesthesia supplemented with Halothane inhalation. The cats were placed in a stereotaxic frame. Two osmotic minipumps (Alzet, model 2002), connected with polyethylene tubing to stainless steel cannulae, were implanted bilaterally beneath the skin of the neck of each animal. One minipump contained the 2.5S subunit of NGF (human recombinant; Genentech), while the other minipump contained only artificial cerebrospinal fluid and served as a control. Previous studies have shown that NGF is stable at 370C for 2 weeks and is released and diffused from the minipump for this 2-week period (18). The NGF was continuously infused at the rate of 0.1 jug/hr through the infusion cannulae, whose tips were inserted 2 mm below the dura and secured to the skull with dental cement, at HorsleyClarke coordinates P-5, L+2. The OD distributions of neurons in both hemispheres were assessed in 11 cats 3 weeks after monocular deprivation. During the first 2 weeks of this deprivation period, NGF was continuously infused into the visual cortex. The dosage of NGF used in this study was chosen on the basis ofan earlier report (19), which showed that application of the same rate and duration of NGF infusion promoted transplant survival and fiber ingrowth within the striatum ofadult rats. For electrophysiology, the animals were anesthetized, paralyzed, and prepared for routine single unit recording with care taken to sample a sufficient volume of cortex in each animal (10, 16, 20, 21). Stimuli were presented and receptive properties were analyzed quantitatively with VAST, a Macintosh-based computer program for electrophysiology (22). OD classes were formed using a modification of the Hubel-Wiesel seven-point scale (23). Cells ofgroup 1 were driven only by the deprived eye; for cells ofgroup 2 there was marked dominance of the deprived eye; for group 3, slight dominance. For cells in group 4 there was no obvious difference between the two eyes. In group 5 the nondeprived eye dominated slightly; in group 6, markedly; and in group 7 the cells were driven only by the nondeprived eye. Neurons that had spontaneous activity but did not show any responses to visual stimuli were rated "U." For comparison, the sampled cells in OD classes of each individual hemisphere were first normalized. Group data of each OD class are shown in OD histograms (see Figs. 1-3) with means and standard error bars. The distributions ofOD classes observed in NGF-treated and control hemispheres were statistically evaluated using a x2 test. To avoid subjective bias of sampling data, we performed blind experiments in four ofthe recorded cats. During both the minipump implantation and recording sessions, the experimenters did not know which minipumps contained NGF or control solution. To examine any apparent pharmacological effects ofNGF on neuronal responses, monocular deprivation andNGF infusion were imposed on another animal for only 12 days, and cortical recordings were performed while the minipump was still delivering NGF. After electrophysiological recording sessions, all animals were perfused transcardially and the brains were fixed and preserved for further anatomical analyses. 6.1% topic match

6.0%

1.4

2002

[132] Effects of dark rearing on phosphorylation of neurotrophin Trk receptors A. Viegi, ..., and L. Maffei European Journal of Neuroscience 2002 - 31 citations - Show abstract - Cite 6.0% topic match

6.0%

2.1

1994

[133] Antibodies to nerve growth factor (NGF) prolong the sensitive period for monocular deprivation in the rat L. Domenici, ..., and L. Maffei NeuroReport 1994 - 63 citations - Show abstract - Cite 6.0% topic match

6.0%

0.4

2003

[134] Nerve growth factor attenuates hippocampal cholinergic deficits and operant learning impairment in rats with entorhinal cortex lesions H. Shimode, ..., and Y. Morita Behavioural Pharmacology 2003 - 8 citations - Show abstract - Cite 6.0% topic match

5.9%

31.3

2003

[135] Neurotrophin secretion: current facts and future prospects V. Lessmann, ..., and M. Malcangio Progress in Neurobiology 2003 - 675 citations - Show abstract - Cite 5.9% topic match

5.9%

1.4

2004

[136] Neurotrophins induce short‐term and long‐term changes of cortical neurotrophin expression S. Patz and P. Wahle European Journal of Neuroscience 2004 - 29 citations - Show abstract - Cite 5.9% topic match

5.9%

18.5

1992

[137] Neurotrophin expression in rat hippocampal slices: A stimulus paradigm inducing LTP in CA1 evokes increases in BDNF and NT-3 mRNAs S. Patterson, ..., and M. Bothwell Neuron 1992 - 589 citations - Show abstract - Cite 5.9% topic match

5.8%

2.4

1995

[138] Regulation of voltage-gated ion channels by NGF and ciliary neurotrophic factor in SK-N-SH neuroblastoma cells S. Lesser and DC Lo Journal of Neuroscience 1995 - 71 citations - Show abstract - Cite 5.8% topic match

5.8%

13.1

1996

[139] Virus-mediated gene transfer into hippocampal CA1 region restores long-term potentiation in brain-derived neurotrophic factor mutant mice. M. Korte, ..., and T. Bonhoeffer Proceedings of the National Academy of Sciences of the United States of America 1996 - 366 citations - Show abstract - Cite 5.8% topic match

5.8%

7.9

2009

[140] A New Aspect of the TrkB Signaling Pathway in Neural Plasticity K. Ohira and M. Hayashi Current Neuropharmacology 2009 - 118 citations - Show abstract - Cite 5.8% topic match

5.6%

8.3

1997

[141] Disruption of a Single Allele of the Nerve Growth Factor Gene Results in Atrophy of Basal Forebrain Cholinergic Neurons and Memory Deficits Karen S. Chen, ..., and H. Phillips The Journal of Neuroscience 1997 - 225 citations - Show abstract - Cite 5.6% topic match

5.6%

46.9

1995

[142] Activation of postsynaptically silent synapses during pairing-induced LTP in CA1 region of hippocampal slice D. Liao, ..., and R. Malinow Nature 1995 - 1380 citations - Show abstract - Cite 5.6% topic match

5.6%

3.2

1995

[143] Nerve Growth Factor Administration Attenuates Cognitive but Not Neurobehavioral Motor Dysfunction or Hippocampal Cell Loss Following Fluid‐Percussion Brain Injury in Rats G. Sinson, ..., and T. Mcintosh Journal of Neurochemistry 1995 - 92 citations - Show abstract - Cite 5.6% topic match

5.6%

3.5

2001

[144] Long‐term potentiation in the dentate gyrus of the rat hippocampus is accompanied by brain‐derived neurotrophic factor‐induced activation of TrkB M. Gooney and M. Lynch Journal of Neurochemistry 2001 - 82 citations - Show abstract - Cite 5.6% topic match

5.5%

2.3

1994

[145] Nerve growth factor-induced ocular dominance plasticity in adult cat visual cortex. Qiang Gu, ..., and Max S. Cynader Proceedings of the National Academy of Sciences of the United States of America 1994 - 68 citations - Show abstract - Cite 5.5% topic match

5.5%

4.8

1998

[146] Neurotrophins induce release of neurotrophins by the regulated secretory pathway. A. Krüttgen, ..., and E. Shooter Proceedings of the National Academy of Sciences of the United States of America 1998 - 126 citations - Show abstract - Cite 5.5% topic match

5.4%

1.1

1995

[147] Nerve growth factor facilitates cholinergic neurotransmission between nucleus basalis and the amygdala in rat: an electrophysiological analysis H. Moises, ..., and L. Williams Journal of Neuroscience 1995 - 31 citations - Show abstract - Cite Abstract: Treatment of rats in vivo with NGF promotes the survival and enhances the neurotransmitter phenotype of basal forebrain cholinergic neurons. We showed recently (Williams et al., 1993) that NGF-induced stimulations of the cholinergic markers ChAT and high-affinity choline uptake are reflected in an enhanced synthesis and release of ACh in terminals fields of basal forebrain cholinergic neurons. The objective of the present study was to determine whether such effects translate into an enhancement in neurotransmission between nucleus basalis neurons and postsynaptic target cells, and therefore are likely to be of physiological significance. Changes in cholinergic neurotransmission after NGF were assessed by comparing the ability of cholinergic pathway activation, produced by electrical stimulation of nucleus basalis or the external capsule, to elicit intracellularly recorded muscarinic responses in basolateral amygdaloid (BLA) neurons in ventral forebrain slice preparations from NGF-treated and control Fischer 344 adult rats. Chronic infusion of NGF for 3 weeks (1.2 micrograms/d, i.c.v.) increased the likelihood of eliciting cholinergic slow depolarizations (slow EPSP) via stimulation of cholinergic pathways in the slice. In addition, the frequency-response curves for generation of the cholinergic slow EPSP by nucleus basalis or external capsule stimulation were shifted approximately twofold to the left and the EF50 values significantly reduced in neurons from NGF-treated slices, compared to those in preparations from vehicle-treated or untreated controls. Treatment with NGF also resulted in a leftward shift in the frequency-response curve for cholinergic pathway-induced blockade of the slow afterhyperpolarization, without change in the maximal inhibitory effect. The NGF-induced enhancement in cholinergic synaptic effectiveness was not accompanied by alterations in the resting membrane properties or intrinsic excitability of BLA pyramidal neurons. Nor did treatment with NGF affect their chemosensitivity or responsiveness to direct postsynaptic applications of the cholinergic carbachol. We conclude from these results that chronic administration of exogenous NGF can facilitate neurotransmission within basal forebrain cholinergic projections in normal adult brain, presumably as a consequence of its ability to stimulate presynaptic mechanisms involved in synthesis and/or release of ACh. 5.4% topic match

5.4%

0.0

2008

[148] NGF Targets Synaptotagmin 4 J. Foley Science Signaling 2008 - 0 citations - Show abstract - Cite 5.4% topic match

5.4%

0.0

2003

[149] NGF-Induced Enhanced Acquisition of a Spatial Learning Task in Young and Old F 344 Rats is Time Dependent A. Santucci and V. Haroutunian Journal Not Provided 2003 - 0 citations - Show abstract - Cite 5.4% topic match

5.3%

1.9

2000

[150] Nerve Growth Factor Activation of the Extracellular Signal-Regulated Kinase Pathway Is Modulated by Ca2+and Calmodulin J. Egea, ..., and J. Comella Molecular and Cellular Biology 2000 - 48 citations - Show abstract - Cite 5.3% topic match

5.3%

1.1

2007

[151] Brain‐derived neurotrophic factor modulates cell excitability in the mouse medial nucleus of the trapezoid body M. Youssoufian and B. Walmsley European Journal of Neuroscience 2007 - 20 citations - Show abstract - Cite 5.3% topic match

5.3%

5.0

2006

[152] Role of the Neurogranin Concentrated in Spines in the Induction of Long-Term Potentiation A. Zhabotinsky, ..., and J. Lisman The Journal of Neuroscience 2006 - 92 citations - Show abstract - Cite 5.3% topic match

5.3%

11.4

2007

[153] Postsynaptic Secretion of BDNF and NT-3 from Hippocampal Neurons Depends on Calcium–Calmodulin Kinase II Signaling and Proceeds via Delayed Fusion Pore Opening Richard Kolarow, ..., and V. Lessmann The Journal of Neuroscience 2007 - 194 citations - Show abstract - Cite Abstract: The mammalian neurotrophins (NTs) NGF, BDNF, NT-3, and NT-4 constitute a family of secreted neuronal growth factors. In addition, NTs are implicated in several forms of activity-dependent synaptic plasticity. Although synaptic secretion of NTs has been described, the intracellular signaling cascades that regulate synaptic secretion of NTs are far from being understood. Analysis of NT secretion at the subcellular level is thus required to resolve the role of presynaptic and postsynaptic NT secretion for synaptic plasticity. Here, we transfected cultures of dissociated rat hippocampal neurons with green fluorescent protein-tagged versions of BDNF and NT-3, respectively, and identified NT vesicles at glutamatergic synapses by colocalization with the cotransfected postsynaptic marker PSD-95 (postsynaptic density-95)-DsRed. Depolarization-induced secretion of BDNF and NT-3 was monitored with live cell imaging. Direct postsynaptic depolarization with elevated K+ in the presence of blockers of synaptic transmission allowed us to investigate the signaling cascades that are involved in the postsynaptic NT vesicle secretion process. We show that depolarization-induced postsynaptic NT secretion is elicited by Ca2+ influx, either via L-type voltage-gated calcium channels or via NMDA receptors. Subsequent release of Ca2+ from internal stores via ryanodine receptors is required for the secretion process. Postsynaptic NT secretion is inhibited in the presence of KN-62 ([4(2S)-2-[(5-isoquinolinylsulfonyl)methylamino]-3-oxo-3-(4-phenyl-1-piperazinyl)propyl] phenyl isoquinolinesulfonic acid ester) and KN-93 (N-[2-[[[3-(4-chlorophenyl)-2-propenyl]methylamino]methyl]phenyl]-N-(2-hydroxyethyl)-4-methoxybenzenesulfonamide), indicating a critical dependence on the activation of α-calcium–calmodulin-dependent protein kinase II (CaMKII). The cAMP/protein kinase A (PKA) signaling inhibitor Rp-cAMP-S impaired NT secretion, whereas elevation of intracellular cAMP levels was without effect. Using the Trk inhibitor k252a, we show that NT-induced NT secretion does not contribute to the NT release process at synapses, and BDNF does not induce its own secretion at postsynaptic sites. Release experiments in the presence of the fluorescence quencher bromphenol blue provide evidence for asynchronous and prolonged fusion pore opening of NT vesicles during secretion. Because fusion pore opening is fast compared with compound release, the speed of NT release seems to be limited by diffusion of NTs out of the vesicle. Together, our results reveal a strong dependence of activity-dependent postsynaptic NT secretion on Ca2+ influx, Ca2+ release from internal stores, activation of CaMKII, and intact PKA signaling, whereas Trk signaling and activation of Na+ channels is not required. 5.3% topic match

5.2%

8.0

1991

[154] NGF improves spatial memory in aged rodents as a function of age W. Fischer, ..., and F. Gage Journal of Neuroscience 1991 - 265 citations - Show abstract - Cite 5.2% topic match

5.2%

3.1

1993

[155] Effects of nerve growth factor on neuronal plasticity of the kitten visual cortex. Giorgio Carmignoto, ..., and L. Maffei The Journal of Physiology 1993 - 99 citations - Show abstract - Cite 5.2% topic match

5.1%

0.4

1994

[156] Effects of nerve growth factor (NGF) in rats with basal forebrain lesions. S. Ogawa, ..., and K. Hayashi Japanese journal of pharmacology 1994 - 13 citations - Show abstract - Cite 5.1% topic match

5.1%

4.3

2002

[157] Long-term potentiation and spatial learning are associated with increased phosphorylation of TrkB and extracellular signal-regulated kinase (ERK) in the dentate gyrus: evidence for a role for brain-derived neurotrophic factor. M. Gooney, ..., and Marina A. Lynch Behavioral neuroscience 2002 - 97 citations - Show abstract - Cite 5.1% topic match

5.0%

10.0

1997

[158] Brain-Derived Neurotrophic Factor Enhances Long-Term Potentiation in Rat Visual Cortex Y. Akaneya, ..., and H. Hatanaka The Journal of Neuroscience 1997 - 272 citations - Show abstract - Cite 5.0% topic match

5.0%

1.1

1994

[159] Expression of trk in MAH cells lacking the p75 low-affinity nerve growth factor receptor is sufficient to permit nerve growth factor-induced differentiation to postmitotic neurons. J. Verdi, ..., and D. Anderson Proceedings of the National Academy of Sciences of the United States of America 1994 - 33 citations - Show abstract - Cite 5.0% topic match

5.0%

9.8

2003

[160] Brain-Derived Neurotrophic Factor Modulation of GABAergic Synapses by Postsynaptic Regulation of Chloride Transport R. A. Wardle and M. Poo The Journal of Neuroscience 2003 - 206 citations - Show abstract - Cite 5.0% topic match

4.9%

None

[161] Neurogranin controls the spatiotemporal pattern of postsynaptic Neurogranin controls the spatiotemporal pattern of postsynaptic Ca2+/CaM signaling. Ca2+/CaM signaling. No author found Journal Not Provided None - 0 citations - Show abstract - Cite 4.9% topic match

4.9%

0.2

1997

[162] Disruption of a Single Allele of the Nerve Growth Factor Gene Results in Atrophy of Basal Forebrain Cholinergic Neurons and Memory Deficits Karen S Chen, ..., and Heidi S. Phillips Journal Not Provided 1997 - 6 citations - Show abstract - Cite Abstract: Administration of nerve growth factor (NGF) to aged or lesioned animals has been shown to reverse the atrophy of basal fore-brain cholinergic neurons and ameliorate behavioral deficits. To examine the importance of endogenous NGF in the survival of basal forebrain cholinergic cells and in spatial memory, mice bearing a disruption mutation in one allele of the NGF gene were studied. Heterozygous mutant mice (ngfϩ/Ϫ) have reduced levels of NGF mRNA and protein within the hippocam-pus and were found to display significant deficits in memory acquisition and retention in the Morris water maze. The behav-ioral deficits observed in NGF-deficient mice were accompanied by both shrinkage and loss of septal cells expressing cholinergic markers and by a decrease in cholinergic innerva-tion of the hippocampus. Infusions of NGF into the lateral ventricle of adult ngfϩ/Ϫ mice abolished the deficits on the water maze task. Prolonged exposure to NGF may be required to induce cognitive effects, because reversal of the acquisition deficit was seen after long (5 weeks) but not short (3 d) infusion. Although NGF administration did not result in any improvement in the number of septal cells labeled for choline acetyltrans-ferase, this treatment did effectively correct the deficits in both size of cholinergic neurons and density of cholinergic innerva-tion of the hippocampus. These findings demonstrate the importance of endogenous NGF for survival and function of basal forebrain cholinergic neurons and reveal that partial depletion of this trophic factor is associated with measurable deficits in learning and memory. The basal forebrain cholinergic system has been shown to play a critical role in learning and memory f unction. Lesions of basal forebrain cholinergic neurons or their projections produce severe memory deficits (for review, see Olton and Wenk, 1987). Nerve growth factor (NGF) is known to promote the survival, sprouting , and phenotypic expression of responsive neuronal populations to various degrees in developing and mature organisms The profound response of basal forebrain cholinergic cells to NGF in various experimental paradigms has suggested that NGF may serve as a target-derived trophic factor to regulate survival or f unction of these neurons (Hefti et al., 1989). Intraventricular inf usions of NGF can rescue axotomized cholinergic cells and reverse associated memory def-NGF inf usions can ameliorate age-related memory deficits and reverse degeneration of basal fore-brain cholinergic cells (Fischer et al., 1987, 1991). These findings on the actions of exogenous NGF have given rise to the hypothesis that NGF … 4.9% topic match

4.7%

3.3

1996

[163] Brain-derived neurotrophic factor blocks long-term depression in rat visual cortex. Y. Akaneya, ..., and H. Hatanaka Journal of neurophysiology 1996 - 93 citations - Show abstract - Cite 4.7% topic match

4.7%

0.0

1990

[164] 125I-beta-nerve growth factor binding is reduced in rat brain after stress exposure. G. Taglialatela, ..., and J. Perez-Polo Journal of neuroscience research 1990 - 1 citations - Show abstract - Cite 4.7% topic match

4.6%

0.7

1995

[165] Involvement of Nerve Growth Factor in Visual Cortex Plasticity Q. Gu Reviews in the Neurosciences 1995 - 22 citations - Show abstract - Cite 4.6% topic match

4.5%

1.1

1997

[166] Action of the neurotrophins on calcium uptake Hao Jiang and G. Guroff Journal of Neuroscience Research 1997 - 29 citations - Show abstract - Cite 4.5% topic match

4.5%

3.4

2000

[167] Effects of Neurotrophins on Cortical Plasticity: Same or Different? C. Lodovichi, ..., and L. Maffei The Journal of Neuroscience 2000 - 84 citations - Show abstract - Cite 4.5% topic match

4.5%

6.7

1989

[168] NGF receptor reexpression and NGF-mediated cholinergic neuronal hypertrophy in the damaged adult neostriatum F. Gage, ..., and A. Bjorklund Neuron 1989 - 240 citations - Show abstract - Cite 4.5% topic match

4.4%

11.9

2005

[169] Neurotrophin-mediated rapid signaling in the central nervous system: mechanisms and functions. R. Blum and A. Konnerth Physiology 2005 - 234 citations - Show abstract - Cite 4.4% topic match

4.4%

9.5

2004

[170] Neurogranin/RC3 Enhances Long-Term Potentiation and Learning by Promoting Calcium-Mediated Signaling Kuo‐ping Huang, ..., and D. Balschun The Journal of Neuroscience 2004 - 189 citations - Show abstract - Cite 4.4% topic match

4.3%

2.5

2005

[171] BDNF Acutely Modulates Synaptic Transmission and Calcium Signalling in Developing Cortical Neurons Jun He, ..., and Qingming Luo Cellular Physiology and Biochemistry 2005 - 48 citations - Show abstract - Cite 4.3% topic match

4.3%

0.0

2016

[172] Molecular mechanisms of the BDNF activity in modulating neuronal structure N. Gödecke https://doi.org/10.24355/DBBS.084-201611210844-0 2016 - 0 citations - Show abstract - Cite Abstract: The adaptive function of the brain is ensured by modifying the neuronal circuits that underlie experience-dependent learning and memory processes. Neuronal plasticity is determined by the correlation of functional and structural changes of synapses or neurons. Modification of neuronal circuits is tightly controlled by extracellular signals maintaining the balance between excitation and inhibition. The neurotrophin BDNF has been implicated to regulate excitatory-inhibitory transmission of synaptic connections by modulating neuronal function and structure of glutamatergic and GABAergic neurons. The current study was aimed at gaining more insights into the role of BDNF in modulating the neuronal structure and function as well as its role during spatial learning by either deprivation or activity-dependent increase of BDNF. The molecular mechanism mediating BDNF function in glutamatergic and GABAergic neurons was addressed by examining changes in TrkB receptor activation upon a loss-of-function approach. TrkB receptor activation is impaired in inhibitory hippocampal neurons in absence of BDNF while excitatory neurons were not affected. Neither BDNF nor Neurotrophin-4 is required in regulating TrkB signalling in excitatory neurons. Analysis of the molecular mechanism in excitatory hippocampal neurons suggests that TrkB signalling is activated by a neurotrophin-independent, zinc-induced transactivation mechanism. Examination of cbdnf knockout mice revealed that in contrast to excitatory pyramidal neurons dentate gyrus granule cells require BDNF for their postnatal growth whereby this is attributed by a BDNF-dependent TrkB receptor activation. Not only the loss of BDNF signalling results in severe deficits in neuronal plasticity but also its elevation can elicit negative consequences. Synaptotagmin IV knockout mice were used as a gain-of-function approach for BDNF. Loss of this trafficking protein results in enhanced exocytosis of BDNF containing dense-core vesicles in response to neuronal activity. This elevated BDNF secretion elicits deficits in spatial learning and memory retention in the MWM. Analysis of the neuronal function revealed that activity-dependent increase of BDNF evoked by wheel running rescued a LTP deficit detected in sedentary SytIV knockout mice. The role of BDNF mediated by TrkB is extremely specific for distinct cell types and its disequilibrium could lead to an impaired neuronal plasticity provoking deficits in learning and memory. 4.3% topic match

4.3%

1.9

1993

[173] Monocular deprivation effects in the rat visual cortex and lateral geniculate nucleus are prevented by nerve growth factor (NGF). II. Lateral geniculate nucleus L. Domenici, ..., and L. Maffei Proceedings of the Royal Society of London. Series B: Biological Sciences 1993 - 59 citations - Show abstract - Cite 4.3% topic match

4.2%

3.5

2013

[174] Chronic intracerebroventricular infusion of nerve growth factor improves recognition memory in the rat Amy M. Birch and Á. Kelly Neuropharmacology 2013 - 38 citations - Show abstract - Cite 4.2% topic match

4.2%

0.7

2009

[175] Activity-dependent translocation of neurogranin to neuronal nuclei. A. Garrido-García, ..., and F. Diez-guerra The Biochemical journal 2009 - 11 citations - Show abstract - Cite 4.2% topic match

4.2%

2.3

1999

[176] Evidence that nerve growth factor influences recent memory through structural changes in septohippocampal cholinergic neurons M. Catherine Gustilo, ..., and V. Koliatsos Journal of Comparative Neurology 1999 - 60 citations - Show abstract - Cite 4.2% topic match

4.2%

6.5

1997

[177] Potentiation of Developing Synapses by Postsynaptic Release of Neurotrophin-4 Xin-hao Wang and M. Poo Neuron 1997 - 177 citations - Show abstract - Cite 4.2% topic match

4.1%

3.3

1992

[178] The localization of nerve growth factor‐like immunoreactivity in the adult rat basal forebrain and hippocampal formation J. Conner, ..., and M. Manthorpe Journal of Comparative Neurology 1992 - 106 citations - Show abstract - Cite 4.1% topic match

4.1%

0.3

1990

[179] Nerve growth factor induces a dose-dependent and long-lasting increase of choline acetyltransferase activity in the septal area and hippocampus of uninjured rats. G. Vantini, ..., and B. Oderfeld‐Nowak Acta neurobiologiae experimentalis 1990 - 12 citations - Show abstract - Cite 4.1% topic match

4.1%

8.1

2022

[180] Regulation of AMPAR trafficking in synaptic plasticity by BDNF and the impact of neurodegenerative disease J. Keifer Journal of Neuroscience Research 2022 - 22 citations - Show abstract - Cite Abstract: Research demonstrates that the neural mechanisms underlying synaptic plasticity and learning and memory involve mobilization of AMPA‐type neurotransmitter receptors at glutamatergic synaptic contacts, and that these mechanisms are targeted during neurodegenerative disease. Strengthening neural transmission occurs with insertion of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptors (AMPARs) into synapses while weakening results from receptor withdrawal. A key player in the trafficking of AMPARs during plasticity and learning is the brain‐derived neurotrophic factor (BDNF) signaling system. BDNF is a neurotrophic factor that supports neuronal growth and is required for learning and memory. Significantly, a primary feature of many neurodegenerative diseases is a reduction in BDNF protein as well as disrupted neuronal surface expression of synaptic AMPARs. The resulting weakening of synaptic contacts leads to synapse loss and neuronal degeneration that underlies the cognitive impairment and dementia observed in patients with progressive neurodegenerative disease such as Alzheimer’s. In the face of these data, one therapeutic approach is to increase BDNF bioavailability in brain. While this has been met with significant challenges, the results of the research have been promising. In spite of this, there are currently no clinical trials to test many of these findings on patients. Here, research showing that BDNF drives AMPARs to synapses, AMPAR trafficking is essential for synaptic plasticity and learning, and that neurodegenerative disease results in a significant decline in BDNF will be reviewed. The aim is to draw attention to the need for increasing patient‐directed clinical studies to test the possible benefits of increasing levels of neurotrophins, specifically BDNF, to treat brain disorders. Much is known about the cellular mechanisms that underlie learning and memory in brain. It can be concluded that signaling by neurotrophins like BDNF and AMPA‐type glutamate receptor synaptic trafficking are fundamental to these processes. Data from animal models and patients reveal that these mechanisms are adversely targeted during neurodegenerative disease and results in memory loss and cognitive decline. A brief summary of our understanding of these mechanisms indicates that it is time to apply this knowledge base directly to development of therapeutic treatments that enhance neurotrophins for brain disorders in patient populations. 4.1% topic match

4.0%

20.8

2002

[181] Postsynaptic Induction of BDNF-Mediated Long-Term Potentiation Y. Kovalchuk, ..., and A. Konnerth Science 2002 - 471 citations - Show abstract - Cite 4.0% topic match

3.9%

0.5

1993

[182] Expression and regulation of neurotrophins and their receptors in hippocampal systems Cynthia Wetmore and L. Olson Hippocampus 1993 - 16 citations - Show abstract - Cite Abstract: During development of the nervous system, cells proliferate, differentiate, and establish functional connections based upon genetic as well as environmental cues. These processes rely on appropriate chemical signaling among a variety of cells rather than on a predetermined intracellular program of cell fate. Widespread expression of neurotrophic factors undoubtedly plays a significant role in establishing appropriate connections between and among the various populations of neurons. The period of cell proliferation in the nervous system is a dynamic one, in that cell death and elimination occur as a consequence of unsuccessful or inappropriate interactions a neuron has with potential synaptic targets (Oppenheim, 1981 ; Cowan et al., 1984; Jacobson, 1991). Competition among neurons for synapse formation and survival depends upon several factors (see Purves and Lichtman, 1985). Development and maintenance of appropriate connections among neurons and their targets depends on synaptic activity as well as on the availability of chemical mediators on the substrate (Letourneau, 1975; Dodd and Jessell, 1988) and target areas. Growing nerve terminals compete for trophic molecules that are produced by target cells in limited amounts (Barde, 1988). Through competition among neurons for limited trophic molecules from central or peripheral sources, efficient pairings are made between the appropriate neurons and their effector organs (Williams and Herrup, 1988; Barde, 1989; Mattson, 1989; Snider and Johnson, 1989). It is now apparent that nerve growth factor (NGF) and related neurotrophic factors (referred to collectively as neurotrophins) are abundantly expressed in neurons of the hippocampal-entorhinal pathways and presumably play important roles in maintaining neuronal phenotype and function in the mature nervous system. However, neurotrophins, most notably NGF, have long been the subject of investigation prior to their localization in the central nervous system (CNS). Most of the definitive studies regarding trophic interactions have been done in other tissues, particularly those of the periphery (Levi-Montalcini, 1966; Thoenen and Barde, 1980; Levi-Montalcini, 1987; Barde, 1989). While first detected in peripheral tissues, NGF also appears to be a factor expressed by a subset of neurons in the central nervous system-most prominently in the hippocampus-and appears to be important in maintaining survival of central cholinergic neurons (Hefti, 1986; Thoenen et al., 1987a). This review briefly highlights some of the significant find- 3.9% topic match

3.9%

0.0

2013

[183] Neurobiology of Learning and Memory C. Callaghan and Á. Kelly Journal Not Provided 2013 - 0 citations - Show abstract - Cite 3.9% topic match

3.9%

2.4

2002

[184] Acute cholinergic rescue of synaptic plasticity in the neurodegenerating cortex of anti‐nerve‐growth‐factor mice Emanuele Pesavento, ..., and A. Cattaneo European Journal of Neuroscience 2002 - 55 citations - Show abstract - Cite 3.9% topic match

3.9%

1.9

1993

[185] Transsynaptic expression of a presynaptic glutamate receptor during hippocampal long-term potentiation. Tania Smirnova, ..., and Jacques J. B. Mallet Science 1993 - 58 citations - Show abstract - Cite 3.9% topic match

3.9%

4.5

1992

[186] High probability opening of NMDA receptor channels by L-glutamate. C. Jahr Science 1992 - 148 citations - Show abstract - Cite 3.9% topic match

3.8%

0.1

1994

[187] TrkA mediates an NGF survival response in NGF-independent sensory neurons but not in parasympathetic neurons. T. Allsopp, ..., and A. Davies Gene therapy 1994 - 4 citations - Show abstract - Cite 3.8% topic match

3.7%

14.5

2002

[188] Brain-Derived Neurotrophic Factor Triggers Transcription-Dependent, Late Phase Long-Term Potentiation In Vivo ElHoucine Messaoudi, ..., and C. Bramham The Journal of Neuroscience 2002 - 320 citations - Show abstract - Cite 3.7% topic match

3.7%

0.7

1995

[189] Specificity of nerve growth factor signaling: Differential patterns of early tyrosine phosphorylation events induced by NGF, EGF, and bFGF D. Blumberg, ..., and S. Feinstein Journal of Neuroscience Research 1995 - 19 citations - Show abstract - Cite Abstract: The specificity of nerve growth factor (NGF) action was examined by comparing early tyrosine phosphorylation events induced by NGF, epidermal growth factor (EGF), and basic fibroblast growth factor (bFGF). In PC12 cells, administration of either the differentiation factor NGF or the mitogenic factor EGF led to tyrosine phosphorylation of multiple polypeptides in the 100–110 kDa size range associated with PI‐3 kinase. However, NGF induced a more prolonged phosphorylation, relative to a transient EGF effect. In contrast, the differentiation factor bFGF failed to induce measurable tyrosine phosphorylation of PI‐3 kinase‐associated proteins. Similarly, NGF but not bFGF induced marked tyrosine phosphorylation of PLCγ, another early signaling molecule, suggesting that multiple pathways exist for promoting differentiation, and/or that these signaling molecules are not essential for differentiation. TrkA signaling was also compared between PC 12 cells and NIH‐3T3 cells heterologously expressing trkA, where receptor activation promotes mitogenesis. In this comparison, significant differences were observed in the tyrosine phosphorylation pattern of PI‐3 kinase‐associated polypeptides, suggesting the existence of cell type‐specific molecular interactions influencing trkA signaling. Mechanistically, NGF stimulation of PC12 cells resulted in a weak or possibly indirect association between trkA and PI‐3 kinase. Furthermore, NGF did not appear to activate or substantially alter the overall level of PI‐3 kinase activity, raising the possibility that ligand‐induced phosphorylation may serve instead to relocalize constitutively active PI‐3 kinase molecules within the cell. Taken together, data presented suggest that the temporal pattern of induced phosphorylation, the nature of induced associations with other phosphoproteins, and cell type‐specific components may all contribute to the generation of NGF signaling specificity. © 1995 Wiley‐Liss, Inc. 3.7% topic match

3.6%

50.6

1995

[190] Hippocampal long-term potentiation is impaired in mice lacking brain-derived neurotrophic factor. M. Korte, ..., and T. Bonhoeffer Proceedings of the National Academy of Sciences of the United States of America 1995 - 1473 citations - Show abstract - Cite 3.6% topic match

3.6%

0.3

1994

[191] Central administration of the excitotoxin N-methyl-D-aspartate increases nerve growth factor mRNA in vivo. J. Springer, ..., and F. Sessler Neurotoxicology 1994 - 9 citations - Show abstract - Cite 3.6% topic match

3.6%

3.0

2007

[192] Neurogranin controls the spatiotemporal pattern of postsynaptic Ca2+/CaM signaling. Yoshihisa Kubota, ..., and M. Waxham Biophysical journal 2007 - 51 citations - Show abstract - Cite 3.6% topic match

3.5%

4.5

2001

[193] Regulated secretion of neurotrophins by metabotropic glutamate group I (mGluRI) and Trk receptor activation is mediated via phospholipase C signalling pathways M. Canossa, ..., and H. Thoenen The EMBO Journal 2001 - 106 citations - Show abstract - Cite 3.5% topic match

3.5%

1.9

1999

[194] Regulation of synaptic function by neurotrophic factors in vertebrates and invertebrates: implications for development and learning. S. E. McKay, ..., and T. Carew Learning & memory 1999 - 48 citations - Show abstract - Cite 3.5% topic match

3.4%

0.6

1999

[195] MAPK and memory R. Walz, ..., and R. Roesler Trends in Neurosciences 1999 - 14 citations - Show abstract - Cite 3.4% topic match

3.4%

12.9

1998

[196] Enhancement of Neurotransmitter Release Induced by Brain-Derived Neurotrophic Factor in Cultured Hippocampal Neurons Yong‐Xin Li, ..., and N. Davidson The Journal of Neuroscience 1998 - 334 citations - Show abstract - Cite 3.4% topic match

3.4%

6.5

1996

[197] Long-term potentiation increases tyrosine phosphorylation of the N-methyl-D-aspartate receptor subunit 2B in rat dentate gyrus in vivo. Kobi Rosenblum, ..., and Gal Richter-Levin Proceedings of the National Academy of Sciences of the United States of America 1996 - 183 citations - Show abstract - Cite 3.4% topic match

3.3%

1.4

2014

[198] Differential contribution of BDNF and NGF to long-term potentiation in the superior cervical ganglion of the rat E. Arias, ..., and F. Cifuentes Neuropharmacology 2014 - 15 citations - Show abstract - Cite 3.3% topic match

3.3%

1.4

2003

[199] Differential effects of cortical neurotrophic factors on development of lateral geniculate nucleus and superior colliculus neurons: anterograde and retrograde actions P. Wahle, ..., and L. Maffei Development 2003 - 30 citations - Show abstract - Cite Abstract: Neurotrophins strongly affect visual system development and plasticity. However, the mode of delivery and targets of neurotrophin action are still under debate. For instance, cortical NT-4/5 (neurotrophin 4/5; Ntf4/5) was shown to rescue lateral geniculate nucleus (LGN) neurons from monocular deprivation-induced atrophy suggesting a retrograde action on thalamic afferents. It is still unclear whether LGN neurons respond to NT-4/5 and other neurotrophins during development in animals with normal vision. We now show that infusions of NT-4/5 and NGF (nerve growth factor) into visual cortex at the onset and the peak of the critical period accelerated LGN neuron growth. BDNF (brain-derived neurotrophic factor) was ineffective. The effects of neurotrophin on LGN development were clearly dissociated from the effects at cortical level because soma growth of cortical layer IV and VI neurons was strongly promoted by BDNF. NT-4/5 was only effective at the onset, but no longer at the peak of the critical period suggesting a switch in neurotrophin dependency for these cortical cell classes. To dissociate retrograde and anterograde effects of the TrkB ligands, we analyzed the stratum griseum superficiale (SGS) of the superior colliculus, a target of visual cortical efferents. Indeed, TrkB-expressing inhibitory SGS neurons responded to cortical NT-4/5 infusion with somatic growth. Strikingly, the TrkB-expressing excitatory tectothalamic calbindin neurons in the SGS did not respond. This demonstrated for the first time a selective cell type-specific anterograde action of NT-4/5 and suggested for the LGN that anterograde as well as retrograde effects contribute to soma size regulation. Strikingly, cortical infusion of the cytokine LIF, which affects development of visual cortex neurochemical architecture, transiently inhibited growth of neurons in LGN, cortical layer IV and VI and SGS. In summary, the study presents three important results. First, central neurons regulate soma size development in an age-and ligand-specific fashion. Second, NT-4/5 and NGF accelerate LGN development in rats with normal vision while LIF delays growth. Third, anterogradely transported NT-4/5 effectively promotes neuronal maturation. These differential actions on subcortical neurons may contribute to the different effects of neurotrophins on visual system development and plasticity. 3.3% topic match

3.2%

0.8

2021

[200] The therapeutic potential of nerve growth factor combined with blood-brain barrier modulation by focused ultrasound for neurodegenerative disorders Kristiana Xhima and I. Aubert Neural Regeneration Research 2021 - 3 citations - Show abstract - Cite 3.2% topic match

3.1%

1.3

1993

[201] Regulation of Nerve Growth Factor mRNA in the Hippocampal Formation: Effects of N-Methyl-d-aspartate Receptor Activation B. Gwag, ..., and J. Springer Experimental Neurology 1993 - 40 citations - Show abstract - Cite 3.1% topic match

3.1%

1.0

1999

[202] Selective up‐regulation of P‐ and R‐type Ca2+ channels in rat embryo motoneurons by BDNF P. Baldelli, ..., and E. Carbone European Journal of Neuroscience 1999 - 25 citations - Show abstract - Cite 3.1% topic match

3.1%

20.4

1991

[203] BDNF mRNA expression is increased in adult rat forebrain after limbic seizures: Temporal patterns of induction distinct from NGF P. J. Isackson, ..., and C. Gall Neuron 1991 - 681 citations - Show abstract - Cite 3.1% topic match

3.1%

1.0

1994

[204] Nerve growth factor (NGF) uptake and transport following injection in the developing rat visual cortex L. Domenici, ..., and L. Maffei Visual Neuroscience 1994 - 29 citations - Show abstract - Cite 3.1% topic match

3.0%

4.0

2018

[205] Nerve Growth Factor Is Responsible for Exercise-Induced Recovery of Septohippocampal Cholinergic Structure and Function Joseph M. Hall, ..., and L. Savage Frontiers in Neuroscience 2018 - 24 citations - Show abstract - Cite 3.0% topic match

2.9%

3.9

1999

[206] Long-Term Enhancement of Central Synaptic Transmission by Chronic Brain-Derived Neurotrophic Factor Treatment N. T. Sherwood and D. Lo The Journal of Neuroscience 1999 - 97 citations - Show abstract - Cite 2.9% topic match

2.9%

3.9

2001

[207] Neurotrophins act at presynaptic terminals to activate synapses among cultured hippocampal neurons C. Collin, ..., and M. Segal European Journal of Neuroscience 2001 - 91 citations - Show abstract - Cite 2.9% topic match

2.9%

4.3

2000

[208] Transgenic mice overexpressing truncated trkB neurotrophin receptors in neurons have impaired long‐term spatial memory but normal hippocampal LTP Tommi Saarelainen, ..., and E. Castrén Synapse 2000 - 103 citations - Show abstract - Cite 2.9% topic match

2.8%

2.7

2012

[209] Cellular Signal Mechanisms of Reward-Related Plasticity in the Hippocampus M. Isokawa Neural Plasticity 2012 - 32 citations - Show abstract - Cite 2.8% topic match

2.8%

9.0

1995

[210] Neurotrophic factors and synaptic plasticity D. Lo Neuron 1995 - 261 citations - Show abstract - Cite 2.8% topic match

2.8%

1.1

2005

[211] Overlap in the distribution of TrkB immunoreactivity and retinohypothalamic tract innervation of the rat suprachiasmatic nucleus G. Allen and D. Earnest Neuroscience Letters 2005 - 22 citations - Show abstract - Cite 2.8% topic match

2.8%

0.3

2006

[212] β2-Adrenoceptor Agonist Clenbuterol Causes NGF Expression and Neuroprotection Yuan Zhu and J. Krieglstein Cns Drug Reviews 2006 - 6 citations - Show abstract - Cite 2.8% topic match

2.8%

9.9

1994

[213] The low affinity NGF receptor, p75, can collaborate with each of the Trks to potentiate functional responses to the neurotrophins P. Hantzopoulos, ..., and G. Yancopoulos Neuron 1994 - 300 citations - Show abstract - Cite 2.8% topic match

2.8%

5.9

1988

[214] Rescue of lesioned septal cholinergic neurons by nerve growth factor: specificity and requirement for chronic treatment CN Montero and Franz Hefti Journal of Neuroscience 1988 - 213 citations - Show abstract - Cite Abstract: We earlier reported that chronic intraventricular injections of NGF into adult rats with partial transection of the fimbria prevent the lesion-induced disappearance of cholinergic neurons in the medial septal nucleus and the diagonal band of Broca (Hefti, 1986). The present study assessed the specificity and treatment requirements of this effect of NGF. Immunohistochemical visualization of NGF receptors (NGF-R) revealed that these molecules are selectively located in forebrain cholinergic neurons of unlesioned brains. Fimbrial transection resulted in transient accumulation of NGF-R in proximal stumps of lesioned axons but failed to induce the expression of NGF-R by other cells in the septal area or near the lesion. Two to three weeks after lesioning, the number of septal neurons expressing NGF-R was reduced by approximately 50% in parallel with the reduction of the number of neurons expressing cholinergic marker enzymes. Repeated intraventricular NGF injections during 4 weeks prevented the disappearance of these cells. Fimbrial transections also reduced the number of septal GABAergic neurons visualized by glutamate decarboxylase immunohistochemistry. The loss of GABAergic neurons was not prevented by NGF. These findings suggest that NGF prevents the lesion-induced degeneration of cholinergic neurons by directly acting on NGF-R expressed by cholinergic cells and that NGF does not affect any neuron with an axonal lesion. Delayed start of the NGF treatment failed to prevent the disappearance of lesioned cholinergic neurons, providing evidence that NGF treatment indeed promotes the survival of these cells rather than simply upregulating the expression of transmitter-specific enzymes. A single injection of NGF at the time of the lesion was not sufficient to prevent the lesion-induced degeneration of cholinergic neurons. Furthermore, termination of chronic NGF treatment after 4 weeks was followed by loss of septal cholinergic neurons after an additional 4 weeks. These findings suggest that the continuous presence of NGF during more than 4 weeks is required to prevent the degeneration of cholinergic cells. The data are discussed in the context of a possible physiological role of NGF in the function of adult forebrain cholinergic neurons. 2.8% topic match

2.7%

1.8

1995

[215] Nerve growth factor (NGF) acutely enhances high-voltage-activated calcium currents in molluscan neurons. W. Wildering, ..., and Andrew G M Bulloch Journal of neurophysiology 1995 - 53 citations - Show abstract - Cite 2.7% topic match

2.7%

0.0

2009

[216] GROWTH FACTOR INDUCES A DOSE-DEPENDENT AND LONG-LASTING INCREASE OF CHOLINE ACETYLTRANSFERASE ACTIVITY IN THE SEPTAL AREA AND HIPPOCARIPUS OF UNINJURED RATS G. Vantini, ..., and B. Oderfeld‐Nowak Journal Not Provided 2009 - 0 citations - Show abstract - Cite Abstract: The effect of nerve growth factor (NGF) on the intact septohippocampal cholinergic system of adult rats was studied. Nerve growth factor was continuously infused at different doses (5-100 pg) for two weeks into the lateral ventricle of adult rats. Controls received intracerebroventricular infusion of equal amounts of cytochrome c. Nerve growth factor treatment was capable of inducing a dose-dependent inorease of choline acetyltransferase activity (ChAT) in septa1 area amd ventral hippocampus. In both areas, the NGF-induced rise of ChAT activity was sustained for at 'least one week after infusion, then it progressively declined towards control values. By three and five weeks, using NGF a t 25 and 100 yg respectively, ChAT ilncrease was still significant in both septum and ventral hippocampus. The present findings corroborate a role for NGF in adult septohippocanpal cholinergic system and indicate that the "pharmacological" modulation of these neurons by NGF may last several weeks following withdrawal of this trophic factor. Increasing body of evidence supports the view that nerve growth factor (NGF) plays a physiological role in the central nervous system (CNS). In this regard, several neurcmal populations are now known to be responsive to NGF including retinal ganglion cells (5, 24), striatal and basal forebrain cholinergic neurons (1, 8, 37). Investigations focused on the action of NGF in the cholinergic systems of the basal forebrain have indicated that (i) a correlation exists between cholinergic innervation in the forebrain anld the distribution of endogenous NGF, its receptor and the mRNA encoding NGF and NGF receptor (4, 9, 19, 20, 23, 32, 40, 45, 46); (ii) biasal forebrain cholinergic neurons of both neonatal and adult rats respond to exogenous NGF with a selective and prominent increase in choline acetyltransferase (ChAT) activity (7, 14, 18, 29), the enzyme involved in the synthesis of acetylcholine; (iii) injury to the septohippampal cholinergic pathway, such as transectioln of the fimbria-fornix, results in changes in the levels of NGF, its mRNA and its receptor (13, 21, 30, 35, 41); (iv) exogenously administered NGF antagonizes the disappearance (andlor death) of axotomized septal cholinergic neurons (15, 22, 30) and (v) intrace~ebroventricular administration of anti-NGF antibodies in neonatal and adult animals produces specific alterations of forebrain cholinergic neurons (12, 39). In addition, we recently showed that contilnuous infusion of NGF for two weeks (via miniosmotic Alzet pumps) in adult CNS, elevates ChAT activity not only in septal cholinergic neurons with a prior lesion but also in unlesioned animals, suggesting that NGF is required for the maintenance and function of mature forebrain cholinergic neurons (11). Furthermore, the effect elicited by NGF is dose-dependent. For example, NGF at 5 yglpump did not significantly increase ChAT activity in septal area. However in the same region NGF at 25 and 50 pglpump increased ChAT activity by 46O/o and 7g0/0, respectively, when compared to control animals (Fig. 1). The increase of ChAT activity induced by 25 pg/pump NGF was sustained for one week; thereafter it declined towards control values. By 3 weeks ChAT increase was less evident but still significant in the septum (Fig. 2). Similar results were obtained in the hippocampus where NGF a t 25 and 50 yglpump was able to elicit a significant incre~ase of ChAT activity (Fig. 1). Also in this area the effect observed using 25 pg NGF was sustained for one week after infusion and then it declined towards control values (Fig. 2). To further investigate the role of NGF on uninjured septohippwampal cholinergic neurons in terms of dose-response effect and maximal duration of the effects on ChAT activity, we have extended our studies by utilizing an NGF dose higher than previously reported. In particular, you~ng adult rats were treated for two weeks with 100 pg NGF and then sacrificed at 7 and 35 days following the terminatian of infusion. At both times, a significa~nt effect of NGF on ChAT activity was observable in the septum and ventral hippwarrrpus (Fig. 3). In both areas the effect 2.7% topic match

2.6%

1.2

1998

[217] Involvement of Ras/MAP kinase in the regulation of Ca2+ channels in adult bullfrog sympathetic neurons by nerve growth factor. S. Lei, ..., and P. Smith Journal of neurophysiology 1998 - 31 citations - Show abstract - Cite 2.6% topic match

2.6%

2.0

1995

[218] TrkA Tyrosine Residues Involved in NGF‐induced Neurite Outgrowth of PC12 Cells N. Inagaki, ..., and D. Lindholm European Journal of Neuroscience 1995 - 60 citations - Show abstract - Cite 2.6% topic match

2.6%

8.6

2010

[219] Neurotrophins and their receptors in early development of the mammalian nervous system. Katarzyna Bartkowska, ..., and R. Djavadian Acta neurobiologiae experimentalis 2010 - 119 citations - Show abstract - Cite 2.6% topic match

2.6%

0.0

1999

[220] [Neuronal growth factors--neurotrophins]. M. Meyer and J. Rasmussen Ugeskrift for laeger 1999 - 1 citations - Show abstract - Cite 2.6% topic match

2.5%

1.0

2003

[221] Differential influence of BDNF and NT3 on the expression of calcium binding proteins and neuropeptide Y in vivo K. Agerman and P. Ernfors NeuroReport 2003 - 21 citations - Show abstract - Cite 2.5% topic match

2.5%

0.0

2007

[222] IN PRESS EGULATION OF GLYCINERGIC AND GABAergic SYNAPTOGENESIS Y BRAIN-DERIVED NEUROTROPHIC FACTOR IN DEVELOPING PINAL NEURONS A. Carrasco, ..., and ND L. G. AGUAYOa Journal Not Provided 2007 - 0 citations - Show abstract - Cite 2.5% topic match

2.5%

5.3

1997

[223] Nerve Growth Factor Modulates Synaptic Transmission between Sympathetic Neurons and Cardiac Myocytes S. T. Lockhart, ..., and S. Birren The Journal of Neuroscience 1997 - 142 citations - Show abstract - Cite 2.5% topic match

2.5%

2.4

2005

[224] BDNF enhancement of postsynaptic NMDA receptors is blocked by ethanol J. E. Kolb, ..., and E. Levine Synapse 2005 - 47 citations - Show abstract - Cite 2.5% topic match

2.4%

0.6

1998

[225] Functional expression of TrkA receptors in hippocampal neurons Lani Aibel, ..., and M. Chao Journal of Neuroscience Research 1998 - 16 citations - Show abstract - Cite 2.4% topic match

2.4%

3.3

1994

[226] Multideterminant role of calcium in hippocampal synaptic plasticity T. Teyler, ..., and Z. Little Hippocampus 1994 - 100 citations - Show abstract - Cite 2.4% topic match

2.4%

0.0

2009

[227] LTP mechanisms in the dentate gyrus in vivo: BDNF signaling, translation control, and gene function Tambudzai Kanhema Journal Not Provided 2009 - 0 citations - Show abstract - Cite 2.4% topic match

2.4%

0.0

2021

[228] Activity‐dependent dysfunctional gene expression patterns are normalized by in vivo treatment of late‐stage Aβ pathology mice with a TrkB/C small molecule ligand Amira Latif‐Hernandez, ..., and F. Longo Alzheimer's & Dementia 2021 - 0 citations - Show abstract - Cite 2.4% topic match

2.3%

0.3

2001

[229] Identification of a novel truncated isoform of trkB in the kitten primary visual cortex F. Forooghian, ..., and S. Prasad Journal of Molecular Neuroscience 2001 - 7 citations - Show abstract - Cite 2.3% topic match

2.3%

0.8

2021

[230] CD40L/CD40 bidirectional signaling is a major regulator of neuronal morphology in the developing nervous system P. Carriba and A. Davies Neural Regeneration Research 2021 - 3 citations - Show abstract - Cite 2.3% topic match

2.3%

3.3

1999

[231] Blockade of NR2B-containing NMDA receptors prevents BDNF enhancement of glutamatergic transmission in hippocampal neurons. R. Crozier, ..., and M. Plummer Learning & memory 1999 - 84 citations - Show abstract - Cite 2.3% topic match

2.2%

0.3

1997

[232] A radioactive binding assay for inhibitors of trkA kinase. E. Knight, ..., and C. Dionne Analytical biochemistry 1997 - 8 citations - Show abstract - Cite 2.2% topic match

2.2%

66.8

1995

[233] Neurotrophins and Neuronal Plasticity H. Thoenen Science 1995 - 1937 citations - Show abstract - Cite 2.2% topic match

2.2%

14.5

2007

[234] The role of neurotrophins in axonal growth, guidance, and regeneration. M. Lykissas, ..., and A. Beris Current neurovascular research 2007 - 253 citations - Show abstract - Cite 2.2% topic match

2.2%

3.2

1985

[235] Neurotrophic activity in the adult rat hippocampal formation: regional distribution and increase after septal lesion F. Collins and K. Crutcher Journal of Neuroscience 1985 - 124 citations - Show abstract - Cite 2.2% topic match

2.2%

8.5

1998

[236] Nerve growth factor: two receptors, multiple functions J. Frade and Y. Barde BioEssays 1998 - 228 citations - Show abstract - Cite 2.2% topic match

2.1%

15.0

1997

[237] Inhibition of GABAA Synaptic Responses by Brain-Derived Neurotrophic Factor (BDNF) in Rat Hippocampus Tatsuro Tanaka, ..., and N. Matsuki The Journal of Neuroscience 1997 - 412 citations - Show abstract - Cite 2.1% topic match

2.1%

32.5

1994

[238] Requirement for BDNF in activity-dependent survival of cortical neurons. Anirvan Ghosh, ..., and M. Greenberg Science 1994 - 993 citations - Show abstract - Cite 2.1% topic match

2.1%

0.0

2023

[239] Title Nerve growth factor and brain-derived neurotrophic factor attenuate angiotensin-II-induced facilitation of calcium channels in acutely dissociated nucleus tractus solitarii neurons of the rat No author found Journal Not Provided 2023 - 0 citations - Show abstract - Cite 2.1% topic match

2.0%

2.1

2006

[240] Promoting neurotrophic effects by GPCR ligands. F. Jeanneteau and M. Chao Novartis Foundation symposium 2006 - 39 citations - Show abstract - Cite Abstract: The neurotrophins-nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), NT-3 and NT-4-represent a family of proteins essential for neuronal survival and plasticity. Each neurotrophin can signal through two different transmembrane receptors, Trk receptor tyrosine kinases and the p75 neurotrophin receptor, the first member of the TNF receptor superfamily. Neurotrophic factors play an important role in neurodegenerative diseases, as well as neuropsychiatric disorders such as depression, bipolar disease and eating disorders. Indeed, a number of approaches have been taken to use neurotrophins to treat Alzheimer's dementia, amyotrophic lateral sclerosis and peripheral sensory neuropathy. However, many of these clinical trails have failed, due to problems in delivery and unforeseen side effects of neurotrophic factors. An alternative approach is to use ligands in the G protein-coupled receptor (GPCR) family to transactivate trophic activities. We have discovered that treatment with adenosine, a neuromodulator that acts through G protein-coupled receptors, is capable of activating Trk tyrosine kinase receptors. Transactivation of neurotrophic receptors by GPCR ligands raise the possibility that small molecules may be used to elicit neurotrophic effects for the treatment of neurodegenerative diseases. This approach would allow for selective targeting of neurons that express specific G protein-coupled receptors and trophic factor receptors. GPCRs transduce information provided by extracellular signals to modulate synaptic activity and neurotransmission. In addition to the classical G protein signalling, GPCR ligands also activate receptor tyrosine kinases (RTK), including neurotrophin receptors. Activation of Trk neurotrophin receptors can occur by GPCR ligands in the absence of neurotrophins. Adenosine and PACAP (pituitary adenylate cyclase activating polypeptide) induce Trk activation specifically through their respective GPCRs to promote cell survival. Transactivation of Trks by GPCRs has emerged as a new theme in the biology of neurotrophin function. Although the precise role of transactivation is unknown, one possibility is that it adds a safety factor that might protect neurons from death in the absence of neurotrophins. Abnormal activity of the neurotrophin system has been implicated in several psychiatric and neurobiological illnesses. However, the lack of knowledge about the precise site of neurotrophin dysfunction has compromised the ability to improve the efficacy and the safety of drugs used in treatment modalities. If small-molecule GPCR ligands can ameliorate neuronal cell loss through Trk, transactivation may offer a new strategy for promoting trophic effects during neurodegeneration. 2.0% topic match

2.0%

18.2

2008

[241] The biology of neurotrophins, signalling pathways, and functional peptide mimetics of neurotrophins and their receptors. S. Skaper CNS & neurological disorders drug targets 2008 - 304 citations - Show abstract - Cite Abstract: The neurotrophins are a family of closely related proteins that were first identified as survival factors for sympathetic and sensory neurons, and have since been shown to control a number of aspects of survival, development and function of neurons in both the central and peripheral nervous systems. Limiting quantities of neurotrophins during development control the numbers of surviving neurons to ensure a match between neurons and the requirement for a suitable density of target innervation. Biological effects of each of the four mammalian neurotrophins are mediated through activation of one or more of the three members of the tropomyosin-related kinase (Trk) family of receptor tyrosine kinases (TrkA, TrkB and TrkC). In addition, all neurotrophins activate the p75 neurotrophin receptor (p75(NTR)), a member of the tumour necrosis factor receptor superfamily. Nerve growth factor (NGF), the best characterised member of the neurotrophin family, sends its survival signals through activation of TrkA and can induce death by binding to p75(NTR). Neurotrophin engagement of Trk receptors leads to activation of Ras, phosphatidylinositol 3-kinase, phospholipase C-gamma1 and signalling pathways controlled through these proteins, including the mitogen-activated protein kinases. Neurotrophin availability is required into adulthood, where they control synaptic function and plasticity, and sustain neuronal cell survival, morphology and differentiation. Preclinical studies point to the therapeutic potential of neurotrophic factors in preventing or slowing the progression of neurodegenerative conditions. Given the difficulties inherent with a protein therapeutic approach to treating central nervous system disorders, increasing attention has turned to the development of alternative strategies and, in particular, small molecule mimetics. This article will provide an overview of neurotrophin biology, their receptors, and signalling pathways, followed by a description of functional mimetics of neurotrophins acting at Trk receptors. Moreover, exciting recent data describing G-protein-coupled receptor transactivation of Trk receptors and their downstream signalling pathways raise the possibility of using small molecules to elicit neuroprotective effects. 2.0% topic match

1.9%

6.7

1999

[242] Molecular mechanisms underlying activity-dependent regulation of BDNF expression. Perry B. Shieh and Anirvan Ghosh Journal of neurobiology 1999 - 169 citations - Show abstract - Cite 1.9% topic match

1.9%

0.3

2004

[243] Behavioral / Systems / Cognitive Neurogranin / RC 3 Enhances Long-Term Potentiation and Learning by Promoting Calcium-Mediated Signaling Kuo‐ping Huang, ..., and D. Balschun Journal Not Provided 2004 - 6 citations - Show abstract - Cite 1.9% topic match

1.9%

None

[244] Presynaptic and Postsynaptic Nmda Receptors Mediate Distinct Effects of Bdnf on Synaptic Transmission Joseph c. Madara and E. Levine Journal Not Provided None - 2 citations - Show abstract - Cite 1.9% topic match

1.9%

0.8

2006

[245] Nerve growth factor affects Ca2+ currents via the p75 receptor to enhance prolactin mRNA levels in GH3 rat pituitary cells Adriana M López-Domínguez, ..., and G. Cota The Journal of Physiology 2006 - 15 citations - Show abstract - Cite 1.9% topic match

1.8%

1.9

1991

[246] Exogenous nerve growth factor stimulates choline acetyltransferase activity in aging Fischer 344 male rats L. R. Williams Neurobiology of Aging 1991 - 64 citations - Show abstract - Cite 1.8% topic match

1.8%

4.3

2004

[247] Protein processing and releases of neuregulin‐1 are regulated in an activity‐dependent manner M. Ozaki, ..., and T. Hashikawa Journal of Neurochemistry 2004 - 87 citations - Show abstract - Cite 1.8% topic match

1.8%

0.1

2005

[248] Enhanced tyrosine phosphorylation of the 2 B subunit of the N-methyl-D-aspartate receptor in long-term potentiation ( synaptic plasticity / protein phosphorylation / hippocampus ) J. Rostas, ..., and T. V. P. BLISSt Journal Not Provided 2005 - 1 citations - Show abstract - Cite Abstract: Both serine/threonine and tyrosine phosphorylation of receptor proteins have been implicated in the process oflong-term potentiation (LTP), but there has been no direct demonstration of a change in receptor phosphorylation after LTP induction. We show that, after induction of LTP in the dentate gyrus of anesthetized adult rats, there is an increase in the tyrosine phosphorylation of the 2B subunit of the N-methyl-D-aspartate (NMDA) receptor (NR2B), as well as several other unidentified proteins. Tyrosine phosphorylation of NR2B was measured in two ways: binding of antiphosphotyrosine antibodies (PY20) to glycoprotein(s) of 180 kDa (GP180) purified on Con A-Sepharose and binding of anti-NR2B antibodies to tyrosine-phosphorylated proteins purified on PY20-agarose. Three hours after LTP induction, anti-NR2B binding to tyrosine phosphorylated proteins, expressed as a ratio of tetanized to control dentate (Tet/Con), was 2.21 ± 0.50 and PY20 binding to GP180 was 1.68 ± 0.16. This increase in the number oftyrosine phosphorylated NR2B subunits occurred without a change in the total number of NR2B subunits. When the induction of LTP was blocked by pretreatment of the animal with the NMDA receptor antagonist MK801, the increase in PY20 binding to GP180 was also blocked (Tet/Con = 1.09 ± 0.26). The increased PY20 binding to GP180 was also apparent 15 min after LTP induction (Tet/Con = 1.41 ± 0.16) but not detectable 5 min after LTP induction (Tet/Con = 1.01 ± 0.19). These results suggest that tyrosine phosphorylation of the NMDA receptor contributes to the maintenance of LTP. Long-term potentiation (LTP) is a form of use-dependent synaptic plasticity that has been proposed as a cellular model for learning (1). The most extensive characterization of the molecular mechanisms involved in the induction and maintenance of LTP has been undertaken in two groups of glutamatergic synapses in mammalian hippocampus: the synapses formed between the axons of the Schaffer collaterals and the dendrites of the pyramidal neurons in the CAl region, which have mainly been investigated in slices in vitro, and the synapses between the axons of the perforant path and the dendrites of the granule cells of the dentate gyrus, which have mainly been investigated in vivo. Induction ofLTP at both of these synapses requires the activation of the N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor and a rise in the intracellular concentration of Ca2+ in the postsynaptic neuron (1-3). This rise in intracellular Ca2+ is believed to activate a series of biochemical events involving changes in protein phosphorylation that result in the induction and maintenance of LTP by mechanisms that may be postand/or presynaptic (1). The case for the involvement of serine/threonine protein kinases in the induction of LTP is strong and based on several lines of evidence. Both broad-spectrum inhibitors of serine/ threonine protein kinases and more selective inhibitors that target the two major Ca2+-activated serine/threonine protein kinases, Ca2+/phospholipid-stimulated protein kinase and Ca2+/calmodulin-stimulated protein kinase II, are able to inhibit the induction of LTP at these synapses (4-8). Furthermore, injection of Ca2+/calmodulin (9) or Ca2+/calmodulinstimulated protein kinase II (10) into CAl pyramidal cells leads to the induction of LTP, and the Ca2+/calmodulinor Ca2+/calmodulin-stimulated protein kinase II-induced and tetanus-induced potentiations occlude one another. Finally, gene knockout mice lacking the gene for the a subunit of Ca2+/calmodulin-stimulated protein kinase II (11) or y subunit of the Ca2+/phospholipid-stimulated protein kinase (12) show greatly impaired or altered LTP, respectively. The evidence for the involvement of tyrosine kinases in LTP induction and/or maintenance is based on the ability of broad-spectrum tyrosine kinase inhibitors to inhibit the induction of a longlasting potentiation (13) and the specific deficits in LTP induction and spatial learning displayed by gene knockout mice lacking the gene for the tyrosine kinase Fyn (14). However, due to the poor selectivity of the tyrosine kinase inhibitors, and the inherent problem with gene knockout experiments that subtle alterations in development and biological compensations may occur, the case for the involvement of tyrosine phosphorylation in LTP induction and/or maintenance is less strong than the case for serine/threonine phosphorylation. The target proteins for these activated protein kinases are not known but there has been a great deal of interest in the possibility that phosphorylation of glutamate receptors might contribute to the expression of LTP (15, 16). Biochemical studies of isolated postsynaptic densities identified a 180-kDa glycoprotein (PSD-GP180) that is highly enriched in these synaptic structures, is phosphorylated in vivo at serine/ threonine and tyrosine residues, and is also phosphorylated in vitro by cAMP-dependent and Ca2+/calmodulin-stimulated protein kinases as well as tyrosine kinases associated with the synaptic apparatus (17-21). The demonstration that the major 180-kDa tyrosine-phosphorylated glycoprotein in postsynaptic densities is the 2B subunit of theNMDA receptor (NR2B) (22) provided an essential link between the earlier biochemical results with PSD-GP180 and the observations implicating protein phosphorylation, including tyrosine phosphorylation, in the modulation of NMDA receptor function (23) and suggested that phosphorylation of NR2B may be particularly important in NMDA receptor regulation. NMDA receptors are heteromeric receptors consisting of the obligatory functional NR1 subunit and one or more members of the NR2 Abbreviations: EPSP, excitatory postsynaptic potential; LTP, longterm potentiation; NMDA, N-methyl-D-aspartate; NR2B, 2B subunit of the NMDA receptor. tTo whom reprint requests should be addressed. e-mail: bcjar@medicine.newcastle.edu.au. 10452 The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. Proc. Natl. Acad. Sci. USA 93 (1996) 10453 family of regulatory subunits of which only the 2A and 2B are present in significant amounts in adult hippocampus (24-28). The observation that stable but selective changes in the tyrosine phosphorylation of PSD-GP180 can be induced under some conditions (29) prompted us to investigate the change in NR2B tyrosine phosphorylation after the induction of LTP. MATERIALS AND METHODS Materials and Antibodies. Con A-Sepharose was purchased from Pharmacia; PY20 (anti-phosphotyrosine mouse monoclonal antibody) was purchased from ICN; PY20-agarose was purchased from Transduction Laboratories (Lexington, KY); phenylmethylsulfonyl fluoride and leupeptin were purchased from Sigma; and enzyme-linked chemiluminescence (ECL) kits were purchased from Amersham. All other reagents were of analytical grade. The mouse monoclonal antibody (GP50), which recognizes the (32 subunit of the Na+/K+-ATPase (K. Sweadner, personal communication) was prepared by Beesley et al. (30). The rabbit polyclonal antibody against NR2B was prepared by immunizing with a synthetic peptide whose sequence was KHSQLSDLYGKFS, corresponding to amino acids 1031-1043 of rat brain NR2B in which this sequence is believed to form part of the intracellular portion of the molecule (22). This sequence was not present in other known subunits of the NMDA receptor and, at the time of immunization, showed no significant homology with any sequence based on nonredundant database searching. The specificity of the antiserum was demonstrated by the following: in adult rat brain, the major immunoreactivity on Western blots was to a band of 180 kDa that was enriched in subcellular fractions enriched in postsynaptic densities and that increased in abundance during development between postnatal days 6 and 16 (J.W.G., A. T. R. Sim, and J.A.P.R., unpublished results); when tested against cell lines transfected with individual NMDA receptor subunits, immunoreactivity was only seen against cells expressing the NR2B subunit (R. Wenthold, personal communication). Electrophysiology. Adult male Sprague-Dawley rats were anesthetized with urethane (1.5 mg/kg, i.p.) and placed in a headholder, and stimulating and recording electrodes were inserted bilaterally into the angular bundle and cell body layer of the dentate gyrus at coordinates 4.4 mm lateral to lamda, and 3.9 mm posterior, 3.0 mm lateral to bregma, respectively. Constant intensity test stimuli were delivered at 30-s intervals throughout the experiment on the tetanized side. Tetanic stimulation (arrows) consisted of three trains (250 Hz for 200 ms), with an intertrain interval of 30 s. The rate of stimulation on the nontetanized side was adjusted to equalize the total number of stimuli delivered to the two sides. To block the induction of LTP, rats were injected with MK801 (2 mg/kg, i.p.) 45 min before the tetanus. Evoked responses were stored to disk, and the slope of the excitatory postsynaptic potential (EPSP) was analyzed off-line using A/DVANCE software. Responses in each experiment were normalized with respect to the mean value obtained in the 20 responses before tetanus. Tissue Preparation and Analysis. Biochemical analyses were performed on single dentate gyri from individual animals that contained 344 ± 8 [kg of protein (mean ± SEM, n = 114; range = 125-550 ,ug). The brain was removed rapidly 5, 15, or 180 min after LTP induction and rapidly cooled to 4°C in a large volume of prechilled 0.32 M sucrose. The dentate gyri were dissected and homogenized in ice-cold 0.32 M sucrose/i mM sodium orthovanadate/100 mM NaF/10 mM sodium pyrophosphate/0.1 mM phenylmethylsulfonyl fluoride/1 mM EGTA/leupeptin (5 ,ug/ml), and an aliquot was taken for protein determination by the method of Lowry et al. (31). Homogenates were diluted with an equal volume o 1.8% topic match

1.8%

6.2

2002

[249] The Role of Neurotrophins in Neurotransmitter Release W. Tyler, ..., and Lucas Pozzo-Miller The Neuroscientist 2002 - 135 citations - Show abstract - Cite 1.8% topic match

1.8%

111.4

2006

[250] Neurotrophin-regulated signalling pathways L. Reichardt Philosophical Transactions of the Royal Society B: Biological Sciences 2006 - 2012 citations - Show abstract - Cite 1.8% topic match

1.8%

0.8

1990

[251] Nerve growth factor and K‐252a increase catecholamine release from PC12 cells B. Nikodijevic, ..., and G. Guroff Journal of Neuroscience Research 1990 - 29 citations - Show abstract - Cite 1.8% topic match

1.8%

48.5

1995

[252] Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor. R. Yao and G. Cooper Science 1995 - 1435 citations - Show abstract - Cite 1.8% topic match

1.7%

0.1

2010

[253] Erratum: Enzyme-inhibitor-like tuning of Ca2+ channel connectivity with calmodulin (Nature (968-972) 463 (2010)) Xiaodong Liu, ..., and D. T. Yue Nature 2010 - 2 citations - Show abstract - Cite 1.7% topic match

1.7%

2.3

2012

[254] Brain-Derived Neurotrophic Factor in Suicide Pathophysiology Yogesh K. Dwivedi https://doi.org/10.1201/b12215-9 2012 - 29 citations - Show abstract - Cite Abstract: Neurotrophins (NTs) are growth factors that are critical in regulating structural, synaptic, and morphological plasticity and in modulating the strength and number of synaptic connections and neurotransmission (Thoenen, 2000). In addition, the role of NTs in the adult central nervous system is important because they participate in the maintenance of neuronal functions, the structural integrity of neurons, and neurogenesis (Cooper et al., 1996), suggesting their biological role during the entire life span. NTs are homodimeric proteins and are categorized into four different classes: nerve growth factor, brain-derived neurotrophic factor (BDNF), NT-3, and NT-4/5. Most functions of NTs are mediated by the tropomycin receptor kinase (Trk) family of tyrosine kinase receptors. The interaction of NTs with the Trk receptors is specific: nerve growth factor binds with TrkA, BDNF and NT-4 both bind to TrkB, and NT-3 binds to TrkC with the highest affinity but can also bind and mediate its actions via TrkA and TrkB receptors. All NTs can bind to the pan75 NT receptor (p75NTR), which plays a role in NT transport, ligand-binding specificity, and Trk functioning (Barbacid, 1994, 1995; Lewin and Barde, 1996; Schweigreiter, 2006). In addition to the full-length TrkB receptor, several noncatalytic truncated TrkB isoforms have also been identified; these isoforms lack the signaling domain, preventing the induction of a signal transduction mechanism. Binding of an NT to the appropriate Trk receptor leads to the dimerization and transphosphorylation of tyrosine residues in the intracellular domain of the Trk receptors and subsequent activation of signaling pathways (Chao et al., 2006; Reichardt, 2006), leading to altered transcription of critical genes.The most widely distributed member of NT family is BDNF (Huang and Reichardt, 2001). The BDNF gene lies on chromosome 11p13 and encodes pro-BDNF, a precursor peptide of mature BDNF (Seidah et al., 1996). BDNF is translated as 30–35 kDa preproproteins consisting of a preprodomain, a prodomain, and a C-terminal mature NT domain. BDNF levels and its intracellular localization in neurons are regulated via several different mechanisms, including BDNF transcripts, messenger RNA (mRNA) and protein transport, and regulated cleavage of pro-BDNF to mature BDNF. The pro-BDNF is produced in the endoplasmic reticulum, which is accumulated in the trans-Golgi network via the Golgi apparatus. Pro-BDNF can be cleaved in the endoplasmic reticulum by furin or in the regulated secretary vesicles by proconvertase enzymes. Pro-BDNF binds to sortilin, an intracellular chaperone that binds to the prodomain of BDNF to traffic it to the regulated secretory pathway, in the Golgi apparatus. This facilitates the correct folding of the mature BDNF domain. The mature domain of BDNF binds to carboxypeptidase E, thereby sorting BDNF to the regulated secretary pathway (Lu et al., 2005). Pro-BDNF can also be processed by serine protease plasmin when pro-BDNF is in the extracellular milieu (Pang et al., 2004). A substitution of valine (Val) to methionine (Met) at codon 66 in the prodomain impairs this sorting of BDNF (Egan et al., 2003). The impact of a BDNF Val66Met polymorphism has been widely studied in relation to the clinical characteristics of suicidal behavior (Zai et al., 2011). 1.7% topic match

1.7%

0.3

1999

[255] Induction of Electrical Excitability by NGF Requires Autocrine Action of a CNTF-like Factor S. S. Lesser, ..., and D. Lo Molecular and Cellular Neuroscience 1999 - 7 citations - Show abstract - Cite 1.7% topic match

1.7%

6.2

1994

[256] Human nerve growth factor improves spatial memory in aged but not in young rats A. Markowska, ..., and D. Olton Journal of Neuroscience 1994 - 188 citations - Show abstract - Cite 1.7% topic match

1.7%

0.9

2000

[257] Actions of brain‐derived neurotrophic factor on evoked and spontaneous EPSCs dissociate with maturation of neurones cultured from rat visual cortex N. Taniguchi, ..., and T. Tsumoto The Journal of Physiology 2000 - 22 citations - Show abstract - Cite Abstract: 1 To address the question of whether brain‐derived neurotrophic factor (BDNF) directly enhances excitatory synaptic transmission, we recorded excitatory postsynaptic currents (EPSCs) from solitary neurones cultured on glial microislands for 7–38 days, and observed changes in EPSCs after the application of BDNF. In this preparation the possible action of BDNF on GABAergic inhibition was not involved, and evoked and spontaneous (miniature) EPSCs were derived from the same group of synapses (autapses). 2 The application of BDNF at a concentration of 200 ng ml−1 rapidly enhanced the frequency of miniature EPSCs (mEPSCs) in almost all the neurones tested. On the other hand, the amplitude of mEPSCs did not change at all, suggesting that the site of BDNF action is presynaptic. 3 In contrast to the enhanced frequency of mEPSCs, evoked EPSCs were not potentiated in 61 % of the cells tested. Most of these BDNF‐insensitive EPSCs had a peak amplitude larger than 1 nA, while most of the other BDNF‐sensitive EPSCs had a smaller amplitude. The former EPSCs had smaller coefficients of variation (CVs) of amplitude, while the latter had larger CVs, suggesting the possibility that the presynaptic release probability for the former groups of EPSCs might have beeen saturated so that the BDNF action was occluded. 4 To test this possibility we applied a low Ca2+ solution to 17 cells and reduced the amplitude of their evoked EPSCs to less than or near to 1 nA. It was found, however, that BDNF did not enhance these EPSCs. Rather, evoked EPSCs of almost all the cells cultured for less than 15 days were enhanced by BDNF, while those of most of the cells cultured for longer than 16 days were not enhanced. 5 These results suggest that BDNF enhances transmitter release from presynaptic sites through its action on the release machinery, which can be differentiated into a BDNF‐insensitive form for evoked release and a BDNF‐sensitive form for spontaneous release with maturation of synapses. 1.7% topic match

1.6%

0.0

2003

[258] Di¡erential in£uence of BDNF and NT3 on the expression of calcium binding proteins and neuropeptideY in vivo K. Agerman and P. Ernfors Journal Not Provided 2003 - 0 citations - Show abstract - Cite 1.6% topic match

1.6%

3.4

2000

[259] Intracellular Ca2+ and Ca2+/Calmodulin-Dependent Kinase II Mediate Acute Potentiation of Neurotransmitter Release by Neurotrophin-3 Xiang-ping He, ..., and B. Lu The Journal of Cell Biology 2000 - 84 citations - Show abstract - Cite 1.6% topic match

1.6%

7.7

2004

[260] Brain‐derived neurotrophic factor induces NMDA receptor subunit one phosphorylation via ERK and PKC in the rat spinal cord S. Slack, ..., and M. Malcangio European Journal of Neuroscience 2004 - 155 citations - Show abstract - Cite 1.6% topic match

1.5%

1.2

1998

[261] Neuronal survival and calcium influx induced by basic fibroblast growth factor in chick ciliary ganglion neurons C. Distasi, ..., and D. Lovisolo European Journal of Neuroscience 1998 - 31 citations - Show abstract - Cite 1.5% topic match

1.5%

3.6

2010

[262] Secreted factors as synaptic organizers E. Johnson-Venkatesh and H. Umemori European Journal of Neuroscience 2010 - 52 citations - Show abstract - Cite 1.5% topic match

1.5%

5.0

1990

[263] Mouse nerve growth factor prevents degeneration of axotomized basal forebrain cholinergic neurons in the monkey V. Koliatsos, ..., and D. Price Journal of Neuroscience 1990 - 171 citations - Show abstract - Cite Abstract: NGF, a trophic polypeptide, is necessary for the normal development and survival of certain populations of neurons in the CNS and PNS. In the CNS, cholinergic neurons of the basal forebrain magnocellular complex (BFMC) are prominent targets of NGF. During rat development, NGF increases the activity of ChAT in these neurons. In adult rats with experimental injury of axons in the fimbria-fornix, NGF prevents degenerative changes in axotomized cholinergic BFMC neurons in the medial septal nucleus (MSN). Because the amino acid sequences of NGF and its receptor (NGF-R) are highly conserved across species, we hypothesized that mouse NGF would also prevent degeneration of cholinergic BFMC neurons in nonhuman primates. Therefore, the present study was designed to test whether fimbria-fornix lesions result in retrograde degenerative changes in basal forebrain cholinergic neurons in macaques, whether these changes are prevented by mouse NGF, and whether the protective effect of NGF is selective for cholinergic neurons of the basal forebrain. Following unilateral complete transection of the fornix, animals were allowed to survive for 2 weeks, during which time half of the subjects received intraventricular NGF in vehicle and the other half received vehicle alone. In animals receiving vehicle alone, there was a 55% reduction in the number of ChAT- immunoreactive cell bodies within the MSN ipsilateral to the lesion; loss of immunoreactive somata was more severe in caudal planes of the MSN. Remaining immunoreactive neurons appeared smaller than those in control, unoperated animals. In Nissl stains, there was no apparent loss of basophilic profiles in the MSN, but cells showed reduced size and intensity of basophilia. Treatment with NGF almost completely prevented reductions in the number and size of cholinergic neurons and had a significant general effect in preventing atrophy in basophilic magnocellular neurons of the MSN, though some basophilic neurons in the MSN did not appear to respond to NGF. Adjacent 7-microns-thick sections stained with ChAT and NGF-R immunocytochemistry revealed that these markers are strictly colocalized in individual neurons in the MSN in controls and in both groups of experimental animals. Thus, mouse NGF profoundly influences the process of axotomy-induced retrograde degeneration in cholinergic BFMC neurons in primates. The in vivo effectiveness of mouse NGF on primate BFMC neurons suggests that mouse or human recombinant NGF may be useful in ameliorating the ACh- dependent, age-associated memory impairments that occur in nonhuman primates.(ABSTRACT TRUNCATED AT 400 WORDS) 1.5% topic match

1.5%

None

[264] Award Number : DAMD 1797-1-7011 TITLE : Brain-Derived Neurotrophic Factor ( BDNF ) and Traumatic Brain Injury ( Head and Spinal ) PRINCIPAL INVESTIGATOR : R. Hicks, ..., and M. Prasad Journal Not Provided None - 0 citations - Show abstract - Cite 1.5% topic match

1.5%

0.0

2015

[265] Nerve growth factor as potential target in central nervous system disorders: A review Priyanka A. Wadke, ..., and N. Mumbai Journal Not Provided 2015 - 0 citations - Show abstract - Cite 1.5% topic match

1.5%

1.7

1987

[266] Nerve growth factor protein level increases in the adult rat hippocampus aftera specific cholinergic lesion L. Lärkfors, ..., and L. Olson Journal of Neuroscience Research 1987 - 64 citations - Show abstract - Cite 1.5% topic match

1.5%

0.9

1999

[267] Role of neurotrophins in neural plasticity: what we learn from the visual cortex. N. Berardi, ..., and L. Maffei Restorative neurology and neuroscience 1999 - 22 citations - Show abstract - Cite 1.5% topic match

1.4%

0.9

2000

[268] Introduction: the unique phenomenon of a distance Ken Goldberg Journal Not Provided 2000 - 22 citations - Show abstract - Cite 1.4% topic match

1.4%

0.5

2002

[269] Neurotrophins and visual cortical plasticity. A. Huberman and A. McAllister Progress in brain research 2002 - 12 citations - Show abstract - Cite 1.4% topic match

1.4%

0.0

2007

[270] Non-Cell-AutonomousRegulationofGABAergicNeuron DevelopmentbyNeurotrophinsandthep75Receptor Jeanine M. Hinterneder and Sarah R Rollor Journal Not Provided 2007 - 0 citations - Show abstract - Cite 1.4% topic match

1.4%

2.1

1999

[271] Activation of p42 mitogen-activated protein kinase by arachidonic acid and trans-1-amino-cyclopentyl-1,3-dicarboxylate impacts on long-term potentiation in the dentate gyrus in the rat: analysis of age-related changes B. McGahon, ..., and M. Lynch Neuroscience 1999 - 53 citations - Show abstract - Cite 1.4% topic match

1.3%

0.0

1993

[272] [Neurotrophins as a therapeutic tool for degenerative neuronal disorders]. S. Furukawa Rinsho shinkeigaku = Clinical neurology 1993 - 1 citations - Show abstract - Cite 1.3% topic match

1.3%

3.1

2010

[273] Nerve Growth Factor Regulates the Firing Patterns and Synaptic Composition of Motoneurons M. A. Davis-López de Carrizosa, ..., and A. Pastor The Journal of Neuroscience 2010 - 45 citations - Show abstract - Cite 1.3% topic match

1.2%

1.4

1996

[274] Responses of basal forebrain cholinergic neurons to damage in the adult brain Z. Henderson Progress in Neurobiology 1996 - 39 citations - Show abstract - Cite 1.2% topic match

1.2%

4.0

2008

[275] Neurotrophins and cytokines in neuronal plasticity. M. Spedding and P. Gressens Novartis Foundation symposium 2008 - 66 citations - Show abstract - Cite 1.2% topic match

1.2%

2.3

2005

[276] Signaling at the vertebrate synapse: new roles for embryonic morphogens? P. Salinas Journal of neurobiology 2005 - 44 citations - Show abstract - Cite 1.2% topic match

1.2%

1.7

2003

[277] Differential effects of fluoxetine and imipramine on the phosphorylation of the transcription factor CREB and cell-viability. J. Koch, ..., and J. Aldenhoff Journal of psychiatric research 2003 - 38 citations - Show abstract - Cite 1.2% topic match

1.2%

2.3

2001

[278] Brain‐derived neurotrophic factor enhances fast excitatory synaptic transmission in human epileptic dentate gyrus W. Zhu and S. Roper Annals of Neurology 2001 - 54 citations - Show abstract - Cite 1.2% topic match

1.2%

2.1

1997

[279] The Effects of Nerve Growth Factor on Spatial Recent Memory in Aged Rats Persist after Discontinuation of Treatment K. Frick, ..., and A. Markowska The Journal of Neuroscience 1997 - 58 citations - Show abstract - Cite 1.2% topic match

1.1%

43.2

1994

[280] The Trk family of neurotrophin receptors. M. Barbacid Journal of neurobiology 1994 - 1295 citations - Show abstract - Cite Abstract: Accumulating evidence indicates that the Trk family of tyrosine protein kinase receptors, Trk (also known as TrkA), TrkB, and TrkC, are responsible for mediating the trophic effects of the NGF family of neurotrophins. Nerve growth factor (NGF) specifically recognizes Trk, a receptor identified in all major NGF targets, including sympathetic, trigeminal, and dorsal root ganglia as well as in cholinergic neurons of the basal forebrain and the striatum. Brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4) specifically activate the TrkB tyrosine kinase receptor. trkB transcripts encoding this receptor are found throughout multiple structures of the central and peripheral nervous system. Neurotrophin-3 (NT-3) primarily activates the TrkC tyrosine protein kinases, four related isoforms encoded by alternative splicing of trkC, a gene also widely expressed throughout the mammalian nervous system. Unlike the other neurotrophins, NT-3 appears to be somewhat promiscuous since it can activate Trk and TrkB kinase receptors, at least in certain cell systems. The trkB and trkC genes also encode noncatalytic neurotrophin receptor isoforms of an as yet, unknown function. Recently, strains of mice lacking each of these tyrosine kinase receptors have been generated. Preliminary characterization of these mutant mice has provided significant information regarding the role of these receptors in the ontogeny of the mammalian nervous system. For instance, mice deficient for Trk receptors lack most sympathetic neurons and do not display nociceptive and temperature sensations, two defects likely to result from severe neuronal cell loss in their trigeminal and dorsal root ganglia. Mice lacking TrkB tyrosine kinase receptors die postnatally due to their inability to intake food. Neuron cell loss in their trigeminal, nodose and petrosal sensory ganglia as well as in the facial motor nucleus are likely to contribute to this phenotype. Finally, TrkC-deficient mice display strikingly abnormal movements consistent with loss of proprioception, a defect likely to be a consequence of the complete loss of Ia muscle afferents observed in this mutant mice. 1.1% topic match

1.1%

0.2

1996

[281] Epidermal growth factor-mediated inhibition of neurotransmitter glutamate release from rat forebrain synaptosomes. A. Barrie, ..., and F. Valtorta Molecular pharmacology 1996 - 7 citations - Show abstract - Cite 1.1% topic match

1.1%

16.0

1994

[282] The role of neurotrophins in the developing nervous system. A. Davies Journal of neurobiology 1994 - 480 citations - Show abstract - Cite 1.1% topic match

1.1%

2.3

1998

[283] Anterograde Transport of Neurotrophin Proteins in the CNS - A Reassessment of the Neurotrophic Hypothesis J. Conner, ..., and C. Gall Reviews in the Neurosciences 1998 - 62 citations - Show abstract - Cite Abstract: The basic tenets of the neurotrophic hypothesis are that i) limiting quantities of a given factor are produced in specific target tissues; ii) responsive neurons projecting to these targets compete for the limiting amounts of the factor; iii) the factor is bound within the target by selective receptors on afferent terminals, internalized, and retrogradely transported to the neuronal cell body where it provides signals affecting neuronal survival and differentiation. Although originally formulated on the basis of evidence for NGF's actions on peripheral sensory and sympathetic neurons, the neurotrophic hypothesis appeared to be upheld for CNS neuronal systems as well, where NGF was found to function primarily as a target-derived trophic factor for basal forebrain cholinergic neurons. With the discovery of additional neurotrophins sharing considerable structural homology with NGF, the question arose of whether the neurotrophic hypothesis held true for all members of this protein family. Recent investigations into the localization and function of neurotrophins other than NGF, particularly BDNF and NT-3, have provided evidence indicating that these molecules may not act in a manner consistent with the neurotrophic hypothesis, as originally postulated. Numerous studies in the peripheral and central nervous systems have now demonstrated that BDNF (and NT-3) may be preferentially trafficked anterogradely along axonal processes and stored within pre-synaptic terminals. Other studies have suggested that these factors may be released in an activity-dependent, rather than constitutive, manner and can act in autocrine or paracrine fashions to subserve an assortment of biological functions including anterograde effects on cell survival and differentiation, as well as more novel roles in synaptic transmission. These recent findings strongly suggest that, while the various neurotrophin proteins may be grouped into a single family based upon their structural homology, they should be considered as a heterogeneous group of trophic factors based upon function and mode of action. 1.1% topic match

1.1%

0.0

1994

[284] Neurotrophin 3potentiates neuronal activity andinhibits y-aminobutyratergic synaptic transmission incortical neurons H. .. Kim Journal Not Provided 1994 - 0 citations - Show abstract - Cite Abstract: Neurotrophins havetraditionally beenre- garded asslowly acting signals essential forneuronal survival anddifferentiation. However, brain-derived neurotrophic fac- torandneurotrophin 3(NT-3) haverecently beenreported to exert anacute potentiation ofsynaptic activity attheamphibian neuromuscular junction. Little isknownabouttheroleof neurotrophins onfunctional synapses inthecentral nervous system. HereweshowthatNT-3rapidly increased thefre- quency ofspontaneous action potentials, anditsynchronized excitatory synaptic activities indeveloping cortical neurons. Moreover, theinhibitory synaptic transmission mediated by -aminobutyric acid (GABA) subtype Areceptors wasfound to bereduced byNT-3.Thus, theexcitatory effects ofNT-3on spontaneous action potentials wereattributable toareduction ofGABAergic transmission. Ourfindings, together withpre- vious reports ofrapid regulation ofcentral nervous system neurotrophin expression byneuronal activity andoftherole of GABAergic transmission incortical plasticity, suggest amech- anismformodulation ofsynaptic transmission andactivity- dependent synaptic modulation incortical neurons. Extensive studies inthepastfewyears haveelucidated the important roles thattheneurotrophins (including nerve growth factor (NGF),brain-derived neurotrophic factor (BDNF), neurotrophin 3(NT-3), andneurotrophin 4/5(NT- 4/5)) playinthedevelopment andmaintenance ofboth peripheral andcentral nervous systems (for recent reviews seerefs. 1and2). Thefunctions ofneurotrophins ondistinct neuronal populations aremediated bythecellular expression ofthetrkfamily oftyrosine kinase receptors (3, 4). While the effects ofneurotrophins onneuronal survival anddifferenti- ation arewellestablished, little isknownabout their role in synaptic development andfunction. Moreover, theclassic viewofneurotrophins stresses their long-lasting, chronic actions. However, arecent study showed that BDNFand NT-3rapidly enhance synaptic activity atdeveloping neuro- muscular junctions inXenopus cell culture (5). Will neuro- trophins also serve asneuromodulators exerting fast regula- tion onsynaptic activity incentral nervous system (CNS) neurons? Neurotrophins andtheir receptors, thetrktyrosine ki- nases, arewidely expressed inthebrain (6-12). Thefact that theexpression ofneurotrophins israpidly enhanced by neuronal activity inCNS (13-22) suggests their rolein activity-dependent processes, suchassynaptic development andplasticity. Inthepresent study, wesought toexamine the acuteeffects ofNT-3ondeveloping cortical synapses in culture, using electrophysiological approaches. Wenowpro- vide direct evidence that NT-3specifically enhances impulse activity inneurons derived fromsomoatosensory cortex and induces synchronization ofexcitatory synaptic currents. Moreover, thepotentiation ofneuronal activity appears tobe attributable toareduction ofyaminobutyric acid (GABA)er- gicsynaptic transmission. Ourresults support thehypothesis that areciprocal regulation between neurotrophin expression andneuronal activity mayoperate tomodulate synaptic efficacy. 1.1% topic match

1.1%

0.8

2011

[285] The role of mesopontine NGF in sleep and wakefulness O. Ramos, ..., and J. Yamuy Brain Research 2011 - 10 citations - Show abstract - Cite 1.1% topic match

1.1%

36.1

1986

[286] Nerve growth factor promotes survival of septal cholinergic neurons after fimbrial transections F. Hefti Journal of Neuroscience 1986 - 1379 citations - Show abstract - Cite 1.1% topic match

1.1%

21.1

1995

[287] Effects of brain-derived neurotrophic factor on optic axon branching and remodelling in vivo S. Cohen-Cory and S. Fraser Nature 1995 - 610 citations - Show abstract - Cite 1.1% topic match

1.1%

0.3

1998

[288] Phosphatidylcholine-specific phospholipase inhibitor D609 differentially affects MAP kinases and immediate-early genes in PC12 cells. Philipp J. Kahle, ..., and A. Verity Cellular signalling 1998 - 9 citations - Show abstract - Cite 1.1% topic match

1.0%

0.5

2001

[289] TrkB‐like immunoreactivity is present on geniculocortical afferents in layer IV of kitten primary visual cortex M. Silver and M. Stryker Journal of Comparative Neurology 2001 - 12 citations - Show abstract - Cite Abstract: Exogenous administration of the neurotrophins brain‐derived neurotrophic factor (BDNF) or neurotrophin‐4/5 (NT‐4/5), or blockade of their endogenous actions, have been reported to affect the anatomic organization and physiological responses of neurons in developing mammalian primary visual cortex. Experimental alteration of levels of these neurotrophic factors can also influence the morphology of the geniculocortical afferents that project from the lateral geniculate nucleus (LGN) to primary visual cortex. BDNF and NT‐4/5 are ligands of the TrkB tyrosine kinase receptor. Although multiple populations of cortical neurons express TrkB, it is not known whether geniculocortical afferents express this receptor on their axon branches in visual cortex. We have anatomically labeled geniculocortical afferents of postnatal day 40 kittens with the anterograde neuronal tracer Phaseolus vulgaris leucoagglutinin (PHA‐L) and performed double‐label immunofluorescence with a panel of anti‐TrkB antibodies. Confocal microscopy and object‐based colocalization analysis were used to measure levels of TrkB‐like immunoreactivity (IR) on geniculocortical afferents in layer IV of primary visual cortex. By using a conservative analysis involving a comparison of measured colocalization with the amount of colocalization expected based on random overlap of TrkB puncta and PHA‐L–labeled afferents, 3 of 5 anti‐TrkB antibodies tested showed significant colocalization with the geniculocortical axons. Results for the other two antibodies were indeterminate. The indices obtained for colocalization of TrkB and geniculocortical afferents were also compared with the equivalent index obtained for GAD65, a protein that has a similar overall expression pattern to that of TrkB but is not expressed on geniculocortical axons. This analysis indicated that TrkB was present on geniculocortical axons for all five TrkB antibodies tested. TrkB‐like IR was also observed on neuronal somata in the LGN. These results indicate that TrkB receptors on geniculocortical afferents are potential mediators of the actions of BDNF and NT‐4/5 in developing visual cortex. J. Comp. Neurol. 436:391–398, 2001. © 2001 Wiley‐Liss, Inc. 1.0% topic match

1.0%

8.4

1990

[290] Nerve growth factor infusion in the primate brain reduces lesion- induced cholinergic neuronal degeneration M. Tuszynski, ..., and F. Gage Journal of Neuroscience 1990 - 284 citations - Show abstract - Cite 1.0% topic match

1.0%

1.3

1995

[291] NGF mRNA is expressed by GABAergic but not cholinergic neurons in rat basal forebrain J. Lauterborn, ..., and C. Gall Journal of Comparative Neurology 1995 - 37 citations - Show abstract - Cite 1.0% topic match

1.0%

14.2

1997

[292] Enlightening the Postsynaptic Density E. Ziff Neuron 1997 - 382 citations - Show abstract - Cite 1.0% topic match

0.9%

0.9

2006

[293] Differential down‐regulation of voltage‐gated calcium channel currents by glutamate and BDNF in embryonic cortical neurons A. Bouron, ..., and Leticia Peris European Journal of Neuroscience 2006 - 17 citations - Show abstract - Cite 0.9% topic match

0.9%

5.6

1999

[294] Characterization of an NGF–P-TrkA Retrograde-Signaling Complex and Age-Dependent Regulation of TrkA Phosphorylation in Sympathetic Neurons Brian A. Tsui-Pierchala and D. Ginty The Journal of Neuroscience 1999 - 141 citations - Show abstract - Cite 0.9% topic match

0.9%

4.1

2012

[295] Intracellular Ca2+ Stores and Ca2+ Influx Are Both Required for BDNF to Rapidly Increase Quantal Vesicular Transmitter Release M. Amaral and Lucas Pozzo-Miller Neural Plasticity 2012 - 51 citations - Show abstract - Cite 0.9% topic match

0.9%

3.4

2012

[296] Neurogranin Targets Calmodulin and Lowers the Threshold for the Induction of Long-Term Potentiation Ling Zhong and N. Gerges PLoS ONE 2012 - 42 citations - Show abstract - Cite 0.9% topic match

0.9%

2.5

1998

[297] Endogenous Neurotrophin-3 Regulates Short-Term Plasticity at Lateral Perforant Path–Granule Cell Synapses M. Kokaia, ..., and O. Lindvall The Journal of Neuroscience 1998 - 64 citations - Show abstract - Cite 0.9% topic match

0.9%

1.5

1995

[298] Differential regulation of catalytic and non-catalytictrkB messenger RNAs in the rat hippocampus following seizures induced by systemic administration of kainate M. Dugich-Djordjevic, ..., and F. Hefti Neuroscience 1995 - 45 citations - Show abstract - Cite 0.9% topic match

0.8%

1.4

2007

[299] Non-Cell-Autonomous Regulation of GABAergic Neuron Development by Neurotrophins and the p75 Receptor Pao-Yen Lin, ..., and S. Birren The Journal of Neuroscience 2007 - 23 citations - Show abstract - Cite 0.8% topic match

0.8%

0.4

2019

[300] Neurogranin Stimulates Ca2+/calmodulin-dependent Kinase II by Inhibiting Calcineurin at Specific Calcium Spike Frequencies Lu Li, ..., and S. Edelstein bioRxiv 2019 - 2 citations - Show abstract - Cite Abstract: Calmodulin sits at the centre of molecular mechanisms underlying learning and memory. Its complex, and sometimes opposite influences, via the binding to various proteins, are yet to be fully understood. Calcium/calmodulin-dependent protein kinase II (CaMKII) and calcineurin (CaN) both bind open calmodulin, favouring Long-term potentiation (LTP) or depression (LTD) respectively. Neurogranin binds to the closed conformation of calmodulin and its impact on synaptic plasticity is less clear. We set up a mechanistic computational model based on allosteric principles to simulate calmodulin state transitions and its interaction with calcium ions and the three binding partners mentioned above. We simulated calcium spikes at various frequencies and show that neurogranin regulates synaptic plasticity along three modalities. At low spike frequencies, neurogranin inhibits the onset of LTD by limiting CaN activation. At intermediate frequencies, neurogranin limits LTP by precluding binding of CaMKII with calmodulin. Finally, at high spike frequencies, neurogranin promotes LTP by enhancing CaMKII autophosphorylation. While neurogranin might act as a calmodulin buffer, it does not significantly preclude the calmodulin opening by calcium. On the contrary, neurogranin synchronizes the opening of calmodulin’s two lobes and promotes their activation at specific frequencies, increasing the chance of CaMKII trans-autophosphorylation. Taken together, our study reveals dynamic regulatory roles played by neurogranin on synaptic plasticity, which provide mechanistic explanations to opposing experimental findings. Author Summary How our brains learn and remember things lies in the subtle changes of the strength with which brain cells connect to each other, the so-called synaptic plasticity. At the level of the recipient neuron, some of the information is encoded into patterns of intracellular calcium spikes. Calmodulin, a small bilobed protein which conformation is regulated by the binding of calcium ions, decodes these signals, and modulates the activity of specific binding partners. Two key regulators, calcineurin and calcium/calmodulin-dependent protein kinase II, which respectively weaken or strengthen synaptic connections, bind both lobes of calmodulin in its open form, favoured by calcium. On the contrary, neurogranin binds preferentially to one lobe of calmodulin, in the closed form, unfavoured by calcium. It was thus initially suggested that it would inhibit calmodulin activation and decrease synaptic plasticity. However, past research showed that neurogranin sometimes actually enhances synaptic plasticity, though the mechanism was unclear. Our computational models showed that neurogranin synchronizes the activation of the two lobes of calmodulin, favouring opening at high frequency calcium spikes. By doing so, neurogranin increases the impact of calmodulin on calcium/calmodulin-dependent protein kinase II and reduces its effect on calcineurin, resulting in a strengthening of synaptic connections. 0.8% topic match

0.8%

24.3

2002

[301] Integration of distributed energy resources. The CERTS Microgrid Concept Robert Lasseter, ..., and J. Eto Lawrence Berkeley National Laboratory 2002 - 554 citations - Show abstract - Cite 0.8% topic match

0.8%

6.2

2004

[302] Expression of TrkA, TrkB and TrkC in human neuroblastomas G. Brodeur, ..., and A. Evans Journal of Neuro-Oncology 2004 - 130 citations - Show abstract - Cite 0.8% topic match

0.8%

3.5

1990

[303] Nerve growth factor infusion into the denervated adult rat hippocampal formation promotes its cholinergic reinnervation T. Hagg, ..., and S. Varon Journal of Neuroscience 1990 - 120 citations - Show abstract - Cite 0.8% topic match

0.8%

3.8

2008

[304] Exercise and Brain Health — Implications for Multiple Sclerosis Lesley J. White and V. Castellano Sports Medicine 2008 - 64 citations - Show abstract - Cite 0.8% topic match

0.8%

0.2

2006

[305] [Stressful events in childhood and psychiatric disorders in the elderly]. L. Bidzan Psychiatria polska 2006 - 3 citations - Show abstract - Cite 0.8% topic match

0.8%

0.3

2000

[306] Neurotrophin-4/5 promotes dendritic outgrowth and calcium currents in cultured mesencephalic dopamine neurons R. A. Defazio, ..., and J. Walsh Neuroscience 2000 - 7 citations - Show abstract - Cite 0.8% topic match

0.7%

1.5

2001

[307] NT-3 regulates BDNF-induced modulation of synaptic transmission in cultured hippocampal neurons Jennifer Paul, ..., and V. Lessmann Neuroreport 2001 - 35 citations - Show abstract - Cite 0.7% topic match

0.7%

0.0

2003

[308] Metaplasticity and the Unified Calcium Model lead to input selectivity in spiking neurons L. Yeung, ..., and H. Shouval Journal Not Provided 2003 - 1 citations - Show abstract - Cite 0.7% topic match

0.7%

14.9

1987

[309] The physiological function of nerve growth factor in the central nervous system: comparison with the periphery. Hans Thoenen, ..., and R. Heumann Reviews of physiology, biochemistry and pharmacology 1987 - 562 citations - Show abstract - Cite 0.7% topic match

0.7%

1.2

1994

[310] Neurotrophic factors and neurologic disease. David M. Holtzman and W. C. Mobley The Western journal of medicine 1994 - 35 citations - Show abstract - Cite 0.7% topic match

0.7%

3.5

1988

[311] Comparison of nerve growth factor's effects on development of septum, striatum, and nucleus basalis cholinergic neurons in vitro J. Hartikka and F. Hefti Journal of Neuroscience Research 1988 - 125 citations - Show abstract - Cite Abstract: In the central nervous system, nerve growth factor (NGF) affects basal forebrain cholinergic neurons during early development and in the adult mammalian brain. These neurons are located in medial septum, diagonal band of Broca, and nucleus basalis of Meynert. While the effects of NGF on the development of septal cholinergic neurons are well documented, only little is known about the influence of NGF on development of cholinergic neurons in the nucleus basalis. In addition to the basal forebrain cholinergic neurons, there are cholinergic interneurons in the corpus striatum, which form an anatomically and functionally distinct population of cholinergic neurons. These striatal interneurons have been reported to respond to NGF during early development; however, it is not known whether the effects of NGF on their development are similar to those on septal cholinergic neurons. We prepared cultures of dissociated cells from fetal rat septum, striatum, and nucleus basalis and investigated the development of cholinergic neurons localized in these three different areas in the presence or absence of NGF. We now report that, first, cholinergic neurons of striatum and nucleus basalis develop a more extensive fiber network and contain more acetylcholinesterase (AChE) per neuron than do cholinergic neurons of septum. The amount of choline acetyltransferase (ChAT) per cholinergic neuron is approximately the same in all three culture types when grown in the absence of NGF. Second, NGF treatment increases and anti‐NGF treatment decreases the number of AChE‐positive neurons in cultures of low plating density, suggesting that NGF is able to promote survival of cholinergic neurons of all three areas studied. Third, NGF increases the total length of fibers and the number of branching points of cholinergic neurons in septal cultures but not in cultures of striatum and nucleus basalis. Fourth, NGF treatment increases AChE activity in septal but not in nucleus basalis or striatal cultures, suggesting that AChE activity reflects the extent of the fiber network of cholinergic neurons of all areas. Fifth, NGF treatment produces severalfold elevations in ChAT activity in septal cultures and more modest increases in cultures of nucleus basalis and striatum, suggesting that NGF is able to stimulate ChAT activity also in the absence of a stimulatory effect on survival and fiber growth. 0.7% topic match

0.7%

22.2

2003

[312] Selectivity in neurotrophin signaling: theme and variations. R. Segal Annual review of neuroscience 2003 - 464 citations - Show abstract - Cite 0.7% topic match

0.7%

1.0

2002

[313] Plasticity in the visual system: role of neurotrophins and electrical activity. L. Maffei Archives italiennes de biologie 2002 - 22 citations - Show abstract - Cite 0.7% topic match

0.7%

0.2

1998

[314] In utero gene transfer reveals survival effects of nerve growth factor on rat brain cholinergic neurones during development A. Martínez-Serrano, ..., and A. Björklund European Journal of Neuroscience 1998 - 6 citations - Show abstract - Cite 0.7% topic match

0.7%

None

[315] Cells and Materials Cells and Materials Silvio Varon, ..., and CA LaJolla Journal Not Provided None - 0 citations - Show abstract - Cite 0.7% topic match

0.6%

4.0

1999

[316] A nerve growth factor mimetic TrkA antagonist causes withdrawal of cortical cholinergic boutons in the adult rat. Thomas Debeir, ..., and Cuello Ac Proceedings of the National Academy of Sciences of the United States of America 1999 - 103 citations - Show abstract - Cite 0.6% topic match

0.6%

9.5

2005

[317] The neurotrophin receptor p75NTR modulates long-term depression and regulates the expression of AMPA receptor subunits in the hippocampus. H. Rösch, ..., and M. Korte Proceedings of the National Academy of Sciences of the United States of America 2005 - 185 citations - Show abstract - Cite 0.6% topic match

0.6%

39.7

2005

[318] Activation of p75NTR by proBDNF facilitates hippocampal long-term depression N. Woo, ..., and B. Lu Nature Neuroscience 2005 - 763 citations - Show abstract - Cite 0.6% topic match

0.6%

2.1

2001

[319] Neonatal olfactory sensory deprivation decreases BDNF in the olfactory bulb of the rat. John H. McLean, ..., and Weldon Bonnell Brain research. Developmental brain research 2001 - 48 citations - Show abstract - Cite 0.6% topic match

0.6%

0.3

2006

[320] Seizure-Induced Neurogenesis in the Dentate Gyrus and its Dependence on Growth Factors and Cytokines H. Scharfman Journal Not Provided 2006 - 6 citations - Show abstract - Cite 0.6% topic match

0.6%

15.9

1992

[321] Health Behavior and Health Education: Theory, Research, and Practice P. Himmel Annals of Internal Medicine 1992 - 522 citations - Show abstract - Cite 0.6% topic match

0.6%

0.6

2007

[322] [Memory coding and retention: brain-derived neurotrophic factor (BDNF) in synaptic plasticity]. A. Gomez-Palacio Schjetnan and M. Escobar-Rodríguez Revista de neurologia 2007 - 10 citations - Show abstract - Cite 0.6% topic match

0.6%

None

[323] The low-affinity p 75 nerve growth factor ( NGF ) receptor mediates NGF-induced tyrosine phosphorylation ( signal transduction ) M. M. Berg, ..., and M. Chao Journal Not Provided None - 1 citations - Show abstract - Cite Abstract: Protein tyrosine phosphorylation is a potential mechanism for initial sinaling in PC12 cells during dfferentiation in response to nerve growth factor (NGF). NGF-induced tyrosine phosphorylation has been found to be initiated by the trk protooncogene, which participates in the formation of highaffinity NGF binding sites. In contrast to transfection of wildtype low-affinity p75 NGF receptors, transfection of p75NGm with mutations in the cytoplasmic domain resulted in an inability of NGF to elicit tyrosine phosphorylation of intracellular substrates, indicating that p75NG is involved in initiating pbosphorylation events by NGF. Even though the p75NGFR receptor does not possess any inherent tyrosne kinase activity, these experiments demonstrate that the p75NGFR has a potential role in NGF-induced tyrosine phosphorylation. Protein tyrosine phosphorylation is initiated by growth factor binding to receptors for insulin, epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF), all of which possess intrinsic tyrosine kinase activity (1). Nerve growth factor (NGF) interacts with a 75-kDa receptor (2) that lacks a cytoplasmic tyrosine kinase domain (3, 4), yet rapid and transient protein tyrosine phosphorylation has been observed upon treatment of PC12 cells with NGF (5-8). The kinase responsible for this activity has been identified as the trk protooncogene, a receptor tyrosine kinase that binds NGF and is activated in PC12 cells, neuroblastoma cells, and embryonic sensory neurons (8, 9, 38). NGF initiates the differentiation and survival of selective neuronal populations by binding to cell surface receptors. In responsive cells, NGF receptors can be divided into two classes differing 100-fold in their rates of dissociation of NGF. The high-affinity form of the receptor, representing lop0 ofthe total number ofbinding sites on responsive cells, binds NGF with a Kd of 10-11 M and mediates the biological effects of NGF on target cells. Gene transfer experiments with the cloned human cDNA (10-12) demonstrated that the low-affinity receptor (Kd = 10-9 M), represented by the p75NGFR receptor protein, is involved in the formation of the high-affinity sites. Affinity crosslinking studies using "'Ilabeled NGF (1251I-NGF) binding in responsive cells suggested that an additional protein was involved in the formation of the high-afflinity NGF receptor complex (13-17). The product of the trk tyrosine kinase has been identified as a low-affinity NGF receptor that participates with p75NGFR to form high-affinity NGF receptors (9, 17). Since p75NGF has been shown to be required for highaffinity NGF binding (10, 17), we have tested whether expression of the p75 low-affinity NGF receptor is required for activation ofprotein tyrosine phosphorylation in response to NGF. Our results indicate that appropriate NGF-induced protein tyrosine phosphorylation requires expression of p75NGFR and that a highly conserved cytoplasmic domain of this receptor is crucial for this response. MATERIALS AND METHODS Cell Culture. PC12 and NR18 cells were maintained in Dulbecco modified Eagle medium (DMEM) with 10%o fetal bovine serum and 5% horse serum (GIBCO). A875 human melanoma cells were maintained in DMEM with 10%6 fetal bovine serum. Constructs. Construction of the deletion mutants of the NGF receptor has been described (15). All cDNAs were subcdoned into the EcoRI site of the pMV7 expression vector and recombinant retroviruses produced as described (18). Retroviral Gene Transfer. Cell lines expressing the wildtype and mutant NGF receptor cDNAs were generated after retroviral infection of helper-free virus stocks. NR18 transfectants were isolated after neomycin (0.5 mg ofG418 per ml; GIBCO) selection and purification by rosetting with the monoclonal antibody ME20.4 and rabbit anti-mouse IgGcoupled human erythrocytes (2, 3, 15). Immunoblotting. Cells were grown to near confluence on 60-mm tissue culture dishes and were serum starved for 1 hr by incubation in serum-free DMEM. The medium was then replaced with DMEM containing 50 ng of NGF per ml or 20 ng ofEGF per ml (Bioproducts for Science, Indianapolis). At the indicated times the cells were rapidly rinsed with ice-cold Tris-buffered saline, solubilized in 120 ,l of sol buffer [10mM Tris hydrochloride, pH 7.4/1% sodium dodecyl sulfate (SDS)/1 mM sodium orthovanadate/0.1 mM sodium molybdate/1 mM phenylmethylsulfonyl fluoride/5 ,ug of aprotinin per ml/5 ,ug of leupeptin per ml], and immediately frozen in dry ice and ethanol. The samples were then boiled for 5 min. Protein concentrations were determined with a protein assay kit (Bio-Rad). Proteins (150 ,ug) were separated by SDS/ PAGE on 6-13% linear gradient polyacrylamide gels (unless otherwise noted) and electrophoretically transferred to nitrocellulose filters as described (19). The filters were incubated with rabbit anti-phosphotyrosine antisera prepared against bacteria expressing v-abl and purified by affinity chromatography as described (19). Labeled proteins were visualized by incubating the filters with 125I-labeled protein A (Amersham) followed by autoradiography on x-ray film with an intensifying screen for 3-5 days, unless otherwise noted. 0.6% topic match

0.5%

1.1

2019

[324] Identification of amino acid residues of nerve growth factor important for neurite outgrowth in human dorsal root ganglion neurons M. Dahlström, ..., and P. Forsell The European Journal of Neuroscience 2019 - 6 citations - Show abstract - Cite 0.5% topic match

0.5%

0.0

2000

[325] Interleukin-6-induced Tyrosine Phosphorylation of Phospholipase C-γ1 in PC12 Cells Young Han Lee, ..., and P. Suh Molecules and Cells 2000 - 1 citations - Show abstract - Cite 0.5% topic match

0.5%

1.3

1997

[326] Calcium currents in dissociated cochlear neurons from the chick embryo and their modification by neurotrophin-3 C. Jiménez, ..., and J. García-Díaz Neuroscience 1997 - 35 citations - Show abstract - Cite 0.5% topic match

0.5%

2.3

2007

[327] Neurotrophins modulate neuron–glia interactions at a vertebrate synapse K. Todd, ..., and R. Robitaille European Journal of Neuroscience 2007 - 41 citations - Show abstract - Cite 0.5% topic match

0.5%

4.9

1997

[328] Reversible schwann cell hyperplasia and sprouting of sensory and sympathetic neurites after intraventricular administration of nerve growth factor J. Winkler, ..., and L. Thal Annals of Neurology 1997 - 136 citations - Show abstract - Cite 0.5% topic match

0.5%

1.5

1999

[329] TrkA activation in the rat visual cortex by antirat trkA IgG prevents the effect of monocular deprivation T. Pizzorusso, ..., and L. Maffei European Journal of Neuroscience 1999 - 39 citations - Show abstract - Cite 0.5% topic match

0.5%

1.2

2004

[330] p75 neurotrophin receptor signaling in the nervous system. Y. Hasegawa, ..., and T. Yamashita Biotechnology annual review 2004 - 25 citations - Show abstract - Cite 0.5% topic match

0.5%

None

[331] Brief Report /calmodulin-dependent Kinase Ii Mediate Acute Potentiation of Neurotransmitter Release by Neurotrophin-3 Intracellular Ca, ..., and Bai Lu Journal Not Provided None - 0 citations - Show abstract - Cite 0.5% topic match

0.5%

0.1

2000

[332] Potential Role for NGF in Breast Cancer H. Hondermarck STEM CELLS 2000 - 2 citations - Show abstract - Cite 0.5% topic match

0.5%

0.8

1992

[333] Effects of bradykinin on cell volume and intracellular pH in NIH 3T3 fibroblasts expressing the ras oncogene M. Ritter, ..., and F. Lang FEBS Letters 1992 - 25 citations - Show abstract - Cite 0.5% topic match

0.5%

0.3

2001

[334] Nerve growth factor induces light adaptive cellular and synaptic plasticity in the outer retina of fish S. Haamedi, ..., and M. Djamgoz Journal of Comparative Neurology 2001 - 8 citations - Show abstract - Cite 0.5% topic match

0.5%

4.0

2022

[335] Neurotrophin Signaling Impairment by Viral Infections in the Central Nervous System Karen Bohmwald, ..., and A. Kalergis International Journal of Molecular Sciences 2022 - 10 citations - Show abstract - Cite 0.5% topic match

0.5%

4.5

2012

[336] Temporal Profiling of Gene Networks Associated with the Late Phase of Long-Term Potentiation In Vivo M. Ryan, ..., and Joanna M. Williams PLoS ONE 2012 - 55 citations - Show abstract - Cite 0.5% topic match

0.4%

2.0

2001

[337] Brain‐derived neurotrophic factor induces long‐lasting potentiation of synaptic transmission in visual cortex in vivo in young rats, but not in the adult Bin Jiang, ..., and T. Tsumoto European Journal of Neuroscience 2001 - 46 citations - Show abstract - Cite 0.4% topic match

0.4%

0.0

2019

[338] Axonal targeting of TrkA and its interacting molecule via transcytosis N. Yamashita and T. Sakurai Proceedings for Annual Meeting of The Japanese Pharmacological Society 2019 - 0 citations - Show abstract - Cite 0.4% topic match

0.4%

1.8

1998

[339] Unilateral hippocampal lesions in newborn and adult rats: effects on spatial memory and BDNF gene expression H. Praag, ..., and I. Black Behavioural Brain Research 1998 - 48 citations - Show abstract - Cite 0.4% topic match

0.4%

13.2

2004

[340] Transactivation of Trk Neurotrophin Receptors by G-Protein-Coupled Receptor Ligands Occurs on Intracellular Membranes R. Rajagopal, ..., and M. Chao The Journal of Neuroscience 2004 - 267 citations - Show abstract - Cite 0.4% topic match

0.4%

0.0

2002

[341] Role of Endogenous BDNF and NT3 for Synaptic Transmission and Plasticity in the Dentate gyrus Klara Olofsdotter Journal Not Provided 2002 - 0 citations - Show abstract - Cite Abstract: The neurotrophins, notably brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3), modulate synaptic transmission and synaptic plasticity in the adult mammalian brain. Recent data suggest that neurotrophins might be mediators of activity-dependent synaptic plasticity. Such plasticity is believed to be a cellular correlate for important processes like learning, but also for diseases, for instance epilepsy. Indeed, reduced levels of endogenous BDNF or NT3 seem to be protective against the development of epilepsy in animal models of the disorder. The aim of this thesis was to study the effect of endogenous BDNF and NT3 on synaptic transmission in an area of the brain that has been proposed to be involved in the development of epilepsy, the dentate gyrus in the hippocampal formation. We did this by using electrophysiological techniques to measure synaptic activity in brain slices from transgenic mice with lowered endogenous levels of BDNF or NT3, by applying BDNF scavenging agents or recombinant BDNF or NT3. Both BDNF and NT3 influenced short-term plasticity of excitatory synaptic transmission onto granule cells in the dentate gyrus. The effects of BDNF and NT3 were input specific. Thus, NT3 modulated synaptic transmission only in synapses between lateral perforant path and granule cells, whereas BDNF affected medial perforant path to granule cell synapses exclusively. Inhibitory synaptic transmission was altered in BDNF but not NT3 deficient mice. The former displayed an increased frequency of action potential independent spontaneous events, and also altered short-term plasticity of evoked inhibitory synaptic transmission. In animals induced to have an experimental form of epilepsy (kindled animals) no differences were observed in inhibitory synaptic transmission between BDNF deficient and wild-type mice. In conclusion, this thesis work shows specific influences of BDNF and NT3 on excitatory and inhibitory synaptic transmission and on short-lasting synaptic plasticity in the dentate gyrus. This would arguably have consequences on the excitability of this system, and could affect the gating properties of the dentate gyrus during epileptogenesis. 0.4% topic match

0.4%

5.2

1987

[342] Basal forebrain magnocellular neurons stain for nerve growth factor receptor: Correlation with cholinergic cell bodies and effects of axotomy J. Springer, ..., and R. Loy Journal of Neuroscience Research 1987 - 196 citations - Show abstract - Cite 0.4% topic match

0.4%

139.1

2006

[343] A specific amyloid-β protein assembly in the brain impairs memory S. Lesné, ..., and K. Ashe Nature 2006 - 2587 citations - Show abstract - Cite 0.4% topic match

0.4%

0.1

2007

[344] Neurotrophin NGF protects glial cells, but not neurons, of stretch receptor of the crayfish Astacus astacus from photooxidative stress A. Lobanov and A. B. Uzdenskii Journal of Evolutionary Biochemistry and Physiology 2007 - 2 citations - Show abstract - Cite 0.4% topic match

0.4%

1.1

2014

[345] Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses D. Standage, ..., and Gunnar Blohm PLoS ONE 2014 - 12 citations - Show abstract - Cite 0.4% topic match

0.4%

5.4

1994

[346] Neurotrophin 3 potentiates neuronal activity and inhibits gamma-aminobutyratergic synaptic transmission in cortical neurons. Han G. Kim, ..., and B. Lu Proceedings of the National Academy of Sciences of the United States of America 1994 - 162 citations - Show abstract - Cite 0.4% topic match

0.4%

6.1

2004

[347] Epigenetic control of neurobehavioural plasticity: the role of neurotrophins I. Branchi, ..., and Enrico Alleva Behavioural Pharmacology 2004 - 123 citations - Show abstract - Cite 0.4% topic match

0.4%

22.3

2002

[348] Mechanism of TrkB-Mediated Hippocampal Long-Term Potentiation L. Minichiello, ..., and M. Korte Neuron 2002 - 492 citations - Show abstract - Cite 0.4% topic match

0.3%

0.7

1994

[349] Staurosporine induces tyrosine phosphorylation of a 145 kDa protein but does not activate gp140trk in PC12 cells. D. Rasouly and P. Lazarovici European journal of pharmacology 1994 - 20 citations - Show abstract - Cite 0.3% topic match

0.3%

4.6

1996

[350] Systemic Administration of a Nerve Growth Factor Conjugate Reverses Age-Related Cognitive Dysfunction and Prevents Cholinergic Neuron Atrophy C. Bäckman, ..., and A. Granholm The Journal of Neuroscience 1996 - 130 citations - Show abstract - Cite 0.3% topic match

0.3%

6.6

1993

[351] BDNF and NT-3 induce intracellular Ca2+ elevation in hippocampal neurones. B. Berninger, ..., and D. Lindholm Neuroreport 1993 - 204 citations - Show abstract - Cite 0.3% topic match

0.3%

6.3

1996

[352] Neurotrophins Stimulate the Release of Dopamine from Rat Mesencephalic Neurons via Trk and p75Lntr Receptors* Andrea Blöchl and C. Sirrenberg The Journal of Biological Chemistry 1996 - 177 citations - Show abstract - Cite 0.3% topic match

0.3%

2.8

1994

[353] Monoclonal antibodies to nerve growth factor affect the postnatal development of the visual system. N. Berardi, ..., and L. Maffei Proceedings of the National Academy of Sciences of the United States of America 1994 - 85 citations - Show abstract - Cite 0.3% topic match

0.3%

2.1

2017

[354] Immunopotentiator Thymosin Alpha-1 Promotes Neurogenesis and Cognition in the Developing Mouse via a Systemic Th1 Bias Ge Wang, ..., and Juntao Zou Neuroscience Bulletin 2017 - 15 citations - Show abstract - Cite 0.3% topic match

0.3%

1.1

2008

[355] Investigation of the functional brain-derived neurotrophic factor gene variant Val66MET in migraine M. Marziniak, ..., and C. Sommer Journal of Neural Transmission 2008 - 18 citations - Show abstract - Cite 0.3% topic match

0.3%

1.0

2018

[356] Ectopic nerve growth factor prevents proliferation in glioma cells by senescence induction D. Meco, ..., and R. Riccardi Journal of Cellular Physiology 2018 - 6 citations - Show abstract - Cite 0.3% topic match

0.3%

6.6

1998

[357] Neurotrophins in the developing and regenerating visual system. C. S. Von Bartheld Histology and histopathology 1998 - 174 citations - Show abstract - Cite 0.3% topic match

0.3%

0.6

2008

[358] The role of Wnt/beta-catenin signaling in postsynaptic differentiation. Jia Wang and Zhen-Ge Luo Communicative & integrative biology 2008 - 10 citations - Show abstract - Cite 0.3% topic match

0.3%

3.1

2001

[359] Ultrastructural localization of brain-derived neurotrophic factor in rat primary sensory neurons Xue-gang Luo, ..., and Xin-Fu Zhou Neuroscience Research 2001 - 74 citations - Show abstract - Cite 0.3% topic match

0.3%

1.5

2000

[360] Trk B signalling controls LTP but not LTD expression in the developing rat visual cortex E. Sermasi, ..., and L. Domenici European Journal of Neuroscience 2000 - 36 citations - Show abstract - Cite 0.3% topic match

0.3%

2.3

2000

[361] Intraparenchymal NGF Infusions Rescue Degenerating Cholinergic Neurons M. Tuszynski Cell Transplantation 2000 - 56 citations - Show abstract - Cite 0.3% topic match

0.3%

0.2

2000

[362] Enhanced Visuospatial Memory Following Intracerebroventricular Administration of Nerve Growth Factor C. Brandner, ..., and F. Schenk Neurobiology of Learning and Memory 2000 - 5 citations - Show abstract - Cite 0.3% topic match

0.3%

1.1

1997

[363] Both p140trk and p75NGFR Nerve Growth Factor Receptors Mediate Nerve Growth Factor-stimulated Calcium Uptake* Hao Jiang, ..., and G. Guroff The Journal of Biological Chemistry 1997 - 30 citations - Show abstract - Cite 0.3% topic match

0.3%

1.1

2013

[364] Neurotrophin Signaling and Alzheimer’s Disease Neurodegeneration − Focus on BDNF/TrkB Signaling J. Wong https://doi.org/10.5772/53364 2013 - 13 citations - Show abstract - Cite 0.3% topic match

0.3%

1.6

1993

[365] Ectopic trkA expression mediates a NGF survival response in NGF- independent sensory neurons but not in parasympathetic neurons T. Allsopp, ..., and Alun M. Davies The Journal of Cell Biology 1993 - 49 citations - Show abstract - Cite 0.3% topic match

0.3%

13.9

1994

[366] BDNF, and NT‐4/5 enhance glutamatergic synaptic transmission in cultured hippocampal neurones V. Lessmann, ..., and R. Heumann NeuroReport 1994 - 414 citations - Show abstract - Cite 0.3% topic match

0.3%

4.2

1998

[367] Growth Factor Receptor Tyrosine Kinases Acutely Regulate Neuronal Sodium Channels through the Src Signaling Pathway M. D. Hilborn, ..., and S. Rane The Journal of Neuroscience 1998 - 112 citations - Show abstract - Cite 0.3% topic match

0.3%

5.2

2010

[368] Dissecting the involvement of tropomyosin-related kinase A and p75 neurotrophin receptor signaling in NGF deficit-induced neurodegeneration S. Capsoni, ..., and A. Cattaneo Proceedings of the National Academy of Sciences 2010 - 74 citations - Show abstract - Cite 0.3% topic match

0.2%

3.0

1988

[369] Nerve growth factor binding in aged rat central nervous system: Effect of acetyl‐l‐carnitine L. Angelucci, ..., and J. Perez-Polo Journal of Neuroscience Research 1988 - 107 citations - Show abstract - Cite 0.2% topic match

0.2%

2.2

2021

[370] CREB3L2 Modulates Nerve Growth Factor-Induced Cell Differentiation Luciana Sampieri, ..., and C. Alvarez Frontiers in Molecular Neuroscience 2021 - 7 citations - Show abstract - Cite 0.2% topic match

0.2%

6.3

1995

[371] TrkA expression in the CNS: evidence for the existence of several novel NGF-responsive CNS neurons David M. Holtzman, ..., and W. C. Mobley Journal of Neuroscience 1995 - 187 citations - Show abstract - Cite 0.2% topic match

0.2%

1.5

2018

[372] Nrf2 deletion results in impaired performance in memory tasks and hyperactivity in mature and aged mice Mark M. Gergues, ..., and G. C. Wagner Brain Research 2018 - 9 citations - Show abstract - Cite 0.2% topic match

0.2%

0.3

2006

[373] Neurotoxicity and pharmacology of Lathyrus sativus extracts of high- and low-toxicity strains K. Kusama‐Eguchi, ..., and Kazuko Watanabe Journal of Natural Medicines 2006 - 5 citations - Show abstract - Cite 0.2% topic match

0.2%

0.5

1998

[374] Effects of elevated levels of nerve growth factor on the septohippocampal system in transgenic mice M. Kawaja, ..., and J. Julien European Journal of Neuroscience 1998 - 14 citations - Show abstract - Cite 0.2% topic match

0.2%

15.0

1998

[375] Neurotrophins Induce Formation of Functional Excitatory and Inhibitory Synapses between Cultured Hippocampal Neurons C. Vicario-Abejón, ..., and M. Segal The Journal of Neuroscience 1998 - 391 citations - Show abstract - Cite 0.2% topic match

0.2%

0.7

2001

[376] Establishment of variant PC12 subclones deficient in stimulation-secretion coupling. Y. Shoji‐Kasai, ..., and M. Takahashi Biochimica et biophysica acta 2001 - 16 citations - Show abstract - Cite 0.2% topic match

0.2%

0.4

1989

[377] Neuronotrophic Factors in Cellular Functional and Cognitive Repair of Adult Brain S. Varon, ..., and M. Manthorpe Pharmacopsychiatry 1989 - 15 citations - Show abstract - Cite 0.2% topic match

0.2%

0.5

2018

[378] The trophic effect of nerve growth factor in primary cultures of rat hippocampal neurons is associated to an anti‐inflammatory and immunosuppressive transcriptional program B. Maino, ..., and S. Cavallaro Journal of Cellular Physiology 2018 - 3 citations - Show abstract - Cite 0.2% topic match

0.2%

1.1

2005

[379] Progression of age‐associated cognitive impairment correlates with quantitative and qualitative loss of TrkA receptor protein in nucleus basalis and cortex H. U. Saragovi Journal of Neurochemistry 2005 - 20 citations - Show abstract - Cite 0.2% topic match

0.2%

3.2

1991

[380] Messenger RNAs for trk and the low-affinity NGF receptor in rat basal forebrain. Marcelo E. Vazquez and Ted Ebendal Neuroreport 1991 - 106 citations - Show abstract - Cite 0.2% topic match

0.2%

2.3

2000

[381] Data and hypotheses on the role of nerve growth factor and other neurotrophins in psychiatric disorders. G. Bersani, ..., and L. Aloe Medical hypotheses 2000 - 55 citations - Show abstract - Cite 0.2% topic match

0.2%

2.7

1999

[382] Brain-Derived Neurotrophic Factor Prevents Low-Frequency Inputs from Inducing Long-Term Depression in the Developing Visual Cortex S. Kinoshita, ..., and T. Tsumoto The Journal of Neuroscience 1999 - 70 citations - Show abstract - Cite 0.2% topic match

0.2%

0.2

1990

[383] Effects of Catecholamines and 4-Methylcatechol on the Synthesis and Secretion of Nerve Growth Factors by Rat Sciatic Nerve Segments in Culture. Ikegami, ..., and Shoei https://doi.org/10.2220/BIOMEDRES.11.61 1990 - 7 citations - Show abstract - Cite Abstract: Epinephrine (EN), norepinephrine (NE), and dopamine (DA) separately increased the nerve growth factor (NGF) content in both the conditioned medium (CM) and cultured rat sciatic nerve segments. The stimulation of the increase in NGF content was observed after an 8-h time lag. These observations suggest that catecholamines stimulate the de nova synthesis and secretion ofNGF protein in organ culture. The maximal effects were observed at limited concentrations such as 0.1-0.2 mM and weakened after 2 days. A similar effect was observed with 4-methylcatechol, a nonamine catechol compound, but not with adrenergic a or ,8 agonists, indicating that adrenergic receptors do not participate in the stimulatory effect. In other words, catecholamines and/or some of their derivatives are able to stimulate NGF synthesis in cultured sciatic nerve. These findings suggest a physiological role for catecholamines and their derivatives to act as a stimulator ofNGF synthesis in end organs that are innervated by sympathetic neurons. Nerve growth factor (NGF) is a neurotrophic factor for sympathetic and sensory neurons in the peripheral nervous system, and for magnocellular cholinergic neurons in the brain (13, 14). NGF is synthesized in innervated end organs and retrogradely transported within the axon into the neuronal cell body. For example, the sciatic nerve is known to be one such pathway ofNGF transportation (13). Recent studies indicate that whereas the sciatic nerve of neonatal and/or young rats has the ability to synthesize NGF, this capability gradually weakens in the adult (10). However, the NGF mRNA level in the adult sciatic nerve ‘To whom correspondence should be addressed becomes markedly elevated after nerve injuries (l0). These facts suggest that NGF is needed for normal neural development and that the factor synthesized after nerve injury plays an important role in the nerve regeneration process. The cells responsible for NGF synthesis in the sciatic nerve are considered to be Schwann cells and fibroblasts, because l) fibroblasts and Schwann cells cultured from sciatic nerve synthesize and secrete NGF into their culture medium (l, 2); and 2) in sim hybridization experiments showed that both cells in sciatic nerve express NGF mRNA in culture (2). In previous studies, we have demonstrated 0.2% topic match

0.2%

0.0

2021

[384] ACD856: A novel positive allosteric modulator of Trk‐signaling in clinical development for the treatment of Alzheimer’s disease G. Nordvall, ..., and P. Forsell Alzheimer's & Dementia 2021 - 0 citations - Show abstract - Cite 0.2% topic match

0.1%

3.4

2012

[385] Loss of NGF-TrkA Signaling from the CNS Is Not Sufficient to Induce Cognitive Impairments in Young Adult or Intermediate-Aged Mice Markus Müller, ..., and L. Minichiello The Journal of Neuroscience 2012 - 41 citations - Show abstract - Cite 0.1% topic match

0.1%

6.0

2004

[386] From modulator to mediator: rapid effects of BDNF on ion channels C. Rose, ..., and A. Konnerth BioEssays 2004 - 119 citations - Show abstract - Cite 0.1% topic match

0.1%

10.1

2014

[387] BDNF: No gain without pain? Peter A. Smith Neuroscience 2014 - 99 citations - Show abstract - Cite 0.1% topic match

0.1%

0.8

1997

[388] Basic fibroblast growth factor-induced seizures in rats Zhao Liu and G. Holmes Neuroscience Letters 1997 - 22 citations - Show abstract - Cite 0.1% topic match

0.1%

2.9

1990

[389] Exogenous Nerve Growth Factor Increases the Activity of High‐Affinity Choline Uptake and Choline Acetyltransferase in Brain of Fisher 344 Male Rats L. R. Williams and R. Rylett Journal of Neurochemistry 1990 - 99 citations - Show abstract - Cite Abstract: Abstract: The objective of this study was to determine the effect of age and chronic intracerebral administration of nerve growth factor (NGF) on the activity of the presynaptic cholinergic neuronal markers hemicholinium‐sensitive high‐affinity choline uptake (HACU) and choline acetyltransferase (ChAT) in the brain of Fisher 344 male rats, in 24‐month‐old rats, a substantial decrease in ChAT activity (30%) was measured in striatum, and decreases in HACU were found in frontal cortex (28%) and hippocampus (23%) compared with 4‐month‐old controls. Cholinergic neurons in brain of both young adult and aged rats responded to administration of exogenous NGF by increased expression of both phenotypes. In 4‐month‐old animals, NGF treatment at 1.2 μg/ day resulted in increased activities of both ChAT and HACU in striatum (175 and 170%, respectively), frontal cortex (133 and 125%), and hippocampus (137 and 125%) compared with untreated and vehicle‐treated 4‐month‐old animals; vehicle treatment had no effect on the activity of either marker. In 24‐month‐old animals treated with NGF for 2 weeks, ChAT activity was increased in striatum (179%), frontal cortex (134%), and hippocampus (119%) compared with 24‐month‐old control animals. Synaptosomal HACU in 24‐month‐old rats was increased in striatum (151%) and frontal cortex (128%) after 2 weeks of NGF treatment, but hippocampal HACU was not significantly different from control values. Treatment of 24‐month‐old rats with NGF for 4 weeks produced further increases in ChAT activity and HACU in striatum and frontal cortex; in hippocampus, the 4‐week treatment did increase HACU, but ChAT activity was not further increased over that produced by 2 weeks of NGF administration. These data indicate an age‐related differential regulation of ChAT activity and HACU between specific brain areas. In addition, NGF stimulated phenotypic expression of these cholinergic markers in both young adult and aged rat brain; there might be an age‐associated differential sensitivity of particular brain regions to exogenous NGF. 0.1% topic match

0.1%

2.9

1999

[390] From visual experience to visual function: roles of neurotrophins. N. Berardi and L. Maffei Journal of neurobiology 1999 - 72 citations - Show abstract - Cite 0.1% topic match

0.1%

0.9

2002

[391] Book Review: Neurotrophins and Plasticity in the Visual Cortex M. Caleo and L. Maffei The Neuroscientist 2002 - 21 citations - Show abstract - Cite 0.1% topic match

0.1%

0.1

2005

[392] Differential role of entorhinal and hippocampal nerve growth factor in short- and long-term memory modulation. R. Walz, ..., and I. Izquierdo Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 2005 - 1 citations - Show abstract - Cite 0.1% topic match

0.1%

0.0

2011

[393] Acute Application of NT-3 on Neonatal Rat Spinal Cords K. Wojcik, ..., and D. Howard Journal Not Provided 2011 - 0 citations - Show abstract - Cite 0.1% topic match

0.1%

0.6

2002

[394] Neurotrophins and plasticity in the visual cortex. M. Caleo and L. Maffei The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry 2002 - 13 citations - Show abstract - Cite 0.1% topic match

0.1%

39.9

1991

[395] The trk proto-oncogene product: a signal transducing receptor for nerve growth factor. D. Kaplan, ..., and L. Parada Science 1991 - 1335 citations - Show abstract - Cite 0.1% topic match

0.1%

0.0

1994

[396] Monoclonal antibodies tonervegrowthfactor affect thepostnatal development ofthevisual system N. Berardi, ..., and L. Maffei Journal Not Provided 1994 - 0 citations - Show abstract - Cite 0.1% topic match

0.1%

31.7

2006

[397] Neurotrophin signalling in health and disease. M. Chao, ..., and F. Lee Clinical science 2006 - 594 citations - Show abstract - Cite 0.1% topic match

0.1%

0.0

2002

[398] Does BDNF Contribute to Temporal Lobe Epilepsy? S. Helen Epilepsy Currents 2002 - 0 citations - Show abstract - Cite 0.1% topic match

0.1%

None

[399] Interplay between glutamate and y-aminobutyric acid transmitter systems in the physiological regulation of brain-derived neurotrophic factor and nerve growth factor synthesis in hippocampal neurons ( gene regulation / neuronal plasticity ) F. Zafra, ..., and D. Lindholm Journal Not Provided None - 14 citations - Show abstract - Cite Abstract: In the central nervous system brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are predominantly located in neurons. Here we demonstrate that the balance between the activity of the glutamatergic and y-aminobutyric acid (GABA)ergic systems controls the physiological levels of BDNF and NGF mRNAs in hippocampal neurons in vitro and in vivo. The blockade of the glutamate receptors and/or stimulation of the GABAergic system reduces BDNF and NGF mRNAs in hippocampus and NGF protein in hippocampus and septum. The reduction ofNGF in the septum reflects the diminished availability of NGF in the projection field of NGF-dependent septal cholinergic neurons. These neurons do not synthesize NGF themselves but accumulate it by retrograde axonal transport. The refined and rapid regulation of BDNF and NGF synthesis by the glutamate and GABA transmitter systems suggests that BDNF and NGF might be involved in activity-dependent synaptic plasticity. Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are two structurally related neurotrophic molecules (1), which are expressed by specific populations of central neurons including pyramidal neurons in the hippocampus proper and granular neurons of the dentate gyrus (2-8). NGF is produced in the hippocampus and is specifically taken up by nerve terminals of cholinergic neurons. The cell bodies of these neurons are localized in the septum, and they accumulate NGF by retrograde axonal transport (9). NGF (10-12) and probably also BDNF (13, 14) promote the survival and maintenance of specialized functions of these septal cholinergic neurons. Glutamate is the major excitatory neurotransmitter in the mammalian brain, whereas y-aminobutyric acid (GABA) mediates the main inhibitory input on neurons. The appropriate balance between the effects of these neurotransmitter systems appears essential for normal neuronal function, and deviations from this balance may lead to seizures and neuronal cell death (15, 16). lonotropic glutamate receptors can, according to pharmacological criteria, be divided into N-methyl-D-aspartate (NMDA) receptors and non-NMDA receptors, which include kainate and a-amino-3-hydroxymethylisoxazole4propionate (AMPA) receptors (17). The normal and pathophysiological functions of these receptors are particularly well studied in the hippocampus. The activation ofNMDA receptors, for example, seems to play a critical role in long-term potentiation (18, 19), whereas uncontrolled hippocampal glutamatereceptor activation leads to seizures and irreversible neuronal damage (15, 16). We have previously shown that depolarization of cultured hippocampal neurons (50 mM KCl) increases both BDNF and NGF mRNA levels in a calcium-dependent manner (20). Of a large number of transmitter substances tested, kainic acid proved the most potent molecule in elevating BDNF and NGF mRNAs in vitro and in vivo (20). However, the use of pharmacological doses of kainic acid (20, 21) or the induction of limbic seizures (22) represents extreme experimental conditions and does not reflect the regulation of the genes of these neurotrophic factors under physiological conditions. We have, therefore, investigated the contribution of the excitatory glutamatergic and the inhibitory GABAergic systems to the physiological regulation of BDNF and NGF synthesis. The results indicate that subtle changes in the balance between the glutamatergic and the GABAergic systems significantly alter expression ofBDNF and NGF in the hippocampus and influence the amount of NGF protein available for the septal cholinergic neurons. MATERIALS AND METHODS Compounds. MK-801 was obtained from Research Biochemicals (Natick, MA). 2,3-Dihydroxy-6-nitrosulfanoylbenzo(f)quinoxaline (NBQX) was from T. Honore from Novo Nordisk (Bagsveard, Denmark). Taq polymerase was obtained from Perkin-Elmer/Cetus, avian myeloblastosis virus reverse transcriptase was from Life Sciences (St. Petersburg, FL), and NuSieve/agarose was from FMC. Dulbecco's modified Eagle's medium and fetal calf serum were obtained from GIBCO. All other reagents were obtained from Sigma. Cell Culture. Neurons were prepared from hippocampi of 17-day-old rat embryos and cultured as described (20). Briefly, isolated hippocampi were incubated for 20 min at 370C in calcium-free and magnesium-free phosphate-buffered saline containing 10 mM glucose, albumin at 1 mg/ml, DNase at 6 ,ug/ml, and papain at 12 units per ml. Hippocampal cells were carefully dissociated with a plastic pipette, collected by centrifugation (900 x g, 5 min), resuspended in Dulbecco's modified Eagle's medium/10%o fetal calf serum, and plated onto plastic culture dishes (0.5 x 106 cells per 35 mm), which were precoated with poly(DL-ornithine) (0.5 mg/ml). Three hours after plating the medium was changed to a serum-free one containing the supplements (except glutamate) as described by Brewer and Cotman (23). RNA Analysis. RNA was extracted by using the guanidinium thiocyanate method (24), glyoxylated, and fractionated on a 1.5% agarose gel (25). A shortened cRNA standard was Abbreviations: BDNF, brain-derived neurotrophic factor; GABA, '-taminobutync acid; NBQX, 2,3-dihydroxy-6nitrosulfanoylbenzo(f)quinoxaline; NGF, nerve growth factor; NMDA, N-methyl-Daspartate. 10037 The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. Proc. Natl. Acad. Sci. USA 88 (1991) added to the samples before extraction to assess RNA recovery. RNA was transferred to Hybond-N filters, which were hybridized with a 32P-labeled mouse BDNF and NGF cRNA probe produced by run-off transcription (20). The filters were later hybridized with a 32P-labeled P-actin probe, and the values were normalized to the 8-actin signal. Quantitative PCR. Neuronal RNA together with a recovery standard were transcribed into cDNA with avian myeloblastosis virus reverse transcriptase followed by 18 amplification cycles by using specific 5' and 3' oligonucleotide primers for NGF. We used 18 cycles because it has been shown (20) that in this system PCR is linear up to 20 cycles. The DNA products were separated on a 3% NuSieve/agarose 3:1 gel and then transferred to filters that were hybridized with a specific mouse NGF cRNA probe (25). Determination of NGF Protein. NGF in hippocampus and septum was measured by a sensitive two-site ELISA (26) with described modifications (27). The mouse monoclonal antibody 27/21 (26) was used for all determinations. All NGF values obtained were corrected for the recovery of added mouse 2.5S NGF. Treatment of Animals. Adult Wistar rats of both sexes weighing 180-200 g were injected i.p. with MK-801, NBQX, or diazepam, or i.v. with muscimol. Control animals received equivalent volumes of physiological saline. Animals treated with bicuculline (i.v.) received one injection of diazepam (10 mg/kg i.p.) after 30 min to suppress seizure activity. At the indicated times rats were decapitated, and brains were quickly removed. Hippocampus and septum were dissected, frozen on dry ice, and stored at -70'C for RNA or protein determination. 0.1% topic match

0.1%

0.8

1991

[400] Identification of tyrosine kinase Trk as a nerve growth factor receptor. A. Ross Cell regulation 1991 - 26 citations - Show abstract - Cite 0.1% topic match

0.1%

0.0

2002

[401] Neurotrophin Depolarization No author found Science's STKE 2002 - 0 citations - Show abstract - Cite 0.1% topic match

0.1%

2.3

2022

[402] Development and Biological Characterization of a Novel Selective TrkA Agonist with Neuroprotective Properties against Amyloid Toxicity Thanasis Rogdakis, ..., and I. Charalampopoulos Biomedicines 2022 - 6 citations - Show abstract - Cite 0.1% topic match

0.1%

0.7

1995

[403] Nerve growth factor preserves behavioral visual acuity in monocularly deprived kittens A. Fiorentini, ..., and L. Maffei Visual Neuroscience 1995 - 22 citations - Show abstract - Cite 0.1% topic match

0.1%

5.5

1995

[404] Somatic gene transfer of NGF to the aged brain: behavioral and morphological amelioration Ks Chen and F. Gage Journal of Neuroscience 1995 - 162 citations - Show abstract - Cite 0.1% topic match

0.1%

16.2

1997

[405] An NGF-TrkA-mediated retrograde signal to transcription factor CREB in sympathetic neurons. A. Riccio, ..., and D. Ginty Science 1997 - 441 citations - Show abstract - Cite 0.1% topic match

0.1%

24.8

1987

[406] Nerve growth factor treatment after brain injury prevents neuronal death. L. F. Kromer Science 1987 - 936 citations - Show abstract - Cite 0.1% topic match

0.1%

3.5

2006

[407] Reduced presynaptic efficiency of excitatory synaptic transmission impairs LTP in the visual cortex of BDNF‐heterozygous mice İ. Abidin, ..., and T. Mittmann European Journal of Neuroscience 2006 - 62 citations - Show abstract - Cite 0.1% topic match

0.1%

4.2

2004

[408] Long-Lasting Rescue of Age-Associated Deficits in Cognition and the CNS Cholinergic Phenotype by a Partial Agonist Peptidomimetic Ligand of TrkA M. Bruno, ..., and H. Saragovi The Journal of Neuroscience 2004 - 84 citations - Show abstract - Cite 0.1% topic match

0.0%

0.5

2003

[409] Memories Are Made of These : From Messengers to Molecules 2 Neurotrophin Expression and Regulation of Neurogenesis during Development C. Brandner Journal Not Provided 2003 - 10 citations - Show abstract - Cite 0.0% topic match

0.0%

0.0

1999

[410] Neuroscience: Neurotrophins as Neurotransmitters No author found Science's STKE 1999 - 0 citations - Show abstract - Cite 0.0% topic match

0.0%

1.2

1995

[411] REVIEW ■ : Neurotrophic Factors and the Specification of Neural Function L. Mendell The Neuroscientist 1995 - 37 citations - Show abstract - Cite 0.0% topic match

0.0%

0.0

2023

[412] Enhanced TrkA signaling impairs basal forebrain-dependent behavior Laura Calvo-Enrique, ..., and Juan Carlos Arévalo Frontiers in Molecular Neuroscience 2023 - 0 citations - Show abstract - Cite 0.0% topic match

0.0%

4.3

1989

[413] Novel neurotrophic factors, receptors, and oncogenes. P. Walicke Annual review of neuroscience 1989 - 155 citations - Show abstract - Cite 0.0% topic match

0.0%

8.7

2020

[414] Focused ultrasound delivery of a selective TrkA agonist rescues cholinergic function in a mouse model of Alzheimer’s disease Kristiana Xhima, ..., and Isabelle Aubert Science Advances 2020 - 42 citations - Show abstract - Cite 0.0% topic match

0.0%

2.6

2001

[415] Neurotrophins differentially enhance acetylcholine release, acetylcholine content and choline acetyltransferase activity in basal forebrain neurons D. Auld, ..., and R. Quirion Journal of Neurochemistry 2001 - 61 citations - Show abstract - Cite Abstract: Several lines of evidence indicate that nerve growth factor is important for the development and maintenance of the basal forebrain cholinergic phenotype. In the present study, using rat primary embryonic basal forebrain cultures, we demonstrate the differential regulation of functional cholinergic markers by nerve growth factor treatment (24–96 h). Following a 96‐h treatment, nerve growth factor (1–100 ng/mL) increased choline acetyltransferase activity (168–339% of control), acetylcholine content (141–185%), as well as constitutive (148–283%) and K+‐stimulated (162–399%) acetylcholine release, but increased release was not accompanied by increased high‐affinity choline uptake. Enhancement of ACh release was attenuated by vesamicol (1 µm), suggesting a vesicular source, and was abolished under choline‐free conditions, emphasizing the importance of extracellular choline as the primary source for acetylcholine synthesized for release. A greater proportion of acetylcholine released from nerve growth factor‐treated cultures than from nerve growth factor‐naïve cultures was blocked by voltage‐gated Ca2+ channel antagonists, suggesting that nerve growth factor modified this parameter of neurotransmitter release. Cotreatment of NGF (20 ng/mL) with K252a (200 nm) abolished increases in ChAT activity and prevented enhancement of K+‐stimulated ACh release beyond the level associated with K252a, suggesting the involvement of TrkA receptor signaling. Also, neurotrophin‐3, neurotrophin‐4 and brain‐derived neurotrophic factor (all at 5–200 ng/mL) increased acetylcholine release, although they were not as potent as nerve growth factor and higher concentrations were required. High brain‐derived neurotrophic factor concentrations (100 and 200 ng/mL) did, however, increase release to a level similar to nerve growth factor. In summary, long‐term exposure (days) of basal forebrain cholinergic neurons to nerve growth factor, and in a less‐potent fashion the other neurotrophins, enhanced the release of acetylcholine, which was dependent upon a vesicular pool and the availability of extracellular choline. 0.0% topic match

0.0%

1.2

1997

[416] Differential Modulation of the Cholinergic Phenotype of the Nucleus Basalis Magnocellularis Neurons by Applying NGF at the Cell Body or Cortical Terminal Fields Linsen Hu, ..., and A. Cuello Experimental Neurology 1997 - 33 citations - Show abstract - Cite Abstract: Although it is well known that exogenous nerve growth factor (NGF) can dramatically affect the phenotype of the basal forebrain cholinergic neurons in normal, aged, or lesioned animals, whether its actions are restricted to the terminal field level of these cholinergic neurons has yet to be established. In most cases, NGF has been applied into the cerebroventricle space giving it access to both the terminal fields and somatodendritic regions. The recent demonstration that TrkA, the essential component of high-affinity NGF receptors, is expressed not only at the distal fields (terminals and distal axons) but also at the proximal fields (cell bodies, dendrites, and proximal axons) of the basal forebrain cholinergic neurons has provoked renewed interest in this problem. More recently, it was further demonstrated that in Alzheimer's disease (AD), the NGF peptide increased throughout the brain but decreased in the nucleus basalis magnocellularis (NBM), suggesting that there is an impaired retrograde transport of NGF from the cortex to the NBM. Thus, it will be crucial to clarify whether or not the TrkA receptors on the somatodendritic fields of the NBM cholinergic neurons respond to exogenous NGF in order to support the rationale for site-directed neurotrophic factor therapy in AD or other neurological disorders. To clarify this issue, we delivered 2.5S purified mouse NGF locally into the cortex or corpus striatum adjacent to the NBM of naive and cortically devascularized mature male Wistar rats. The local distribution of exogenous NGF was demonstrated by immunohistochemical staining. In naive rats, an NGF dose of 84.00 or 16.80 microg infused into either the cortex or the corpus striatum for 2 weeks caused ipsilateral hypertrophy of the cholinergic neurons of the NBM. In cortically devascularized animals, an NGF dose of 84.00 microg delivered into the cortex and 84.00 microg or 16.80 microg infused into the striatum adjacent to the NBM for 2 weeks rescued the ipsilateral cholinergic phenotype of NBM neurons of the basolocortical pathway from retrograde degeneration. Thus, exogenous NGF can affect the cholinergic phenotype of the NBM regardless of whether it is presented to their nerve terminal fields or their somatodendritic region. The present results provide new evidence that the TrkA receptors present in the somatodendritic region of the cholinergic neurons of the NBM are functional and capable of modulating neuronal phenotype in the naive and lesioned CNS, when applied pharmacologically. 0.0% topic match

0.0%

6.1

2018

[417] The brain-derived neurotrophic factor in neuronal plasticity and neuroregeneration: new pharmacological concepts for old and new drugs S. Habtemariam Neural Regeneration Research 2018 - 39 citations - Show abstract - Cite Abstract: Neurotrophins: Neurotrophins are peptides or proteins that are known to regulate neuronal viability, development, and function. Beyond synaptic plasticity, neurotrophins protect neurons from apoptosis and also promote neurogenesis to recover neuronal deficit even in adulthood. For various reasons that we have highlighted previously (Habtemariam, 2016a), neuronal cells in the brain are highly susceptible to oxidative stress and hence efficient cell survival mechanisms must be maintained at all times. Many age-related and other neurodegenerative diseases (NDs) in the brain are also associated with excessive oxidative damage resulting from either high production of reactive oxygen species generated by neurotoxic agents (e.g., amyloid beta (Aβ)) or suppressed level of antioxidant defenses. Our progress in understanding neurotrophins in recent years has now offered more insight into therapeutic options for various NDs where neuroregeneration is considered the best therapeutic approach. This include traumatic brain injury (TBI), Alzheimer’s disease (AD) and Parkinson’s disease (PD), among others. Neurotrophins that have been well-characterised to date include the nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5). Among the neurotrophins, BDNF is the best studied with explosive number of publications appeared in the last decade to establish its functional role in the brain and targeting it to treat for many diseases. Upon binding to its receptor, a signal transduction pathway that is common to the process of cell proliferation promotion and/or inhibition of the apoptosis cascade has been shown to be activated. Not surprisingly, the common mitogen activated protein kinase (MAPK) pathway, particularly the extracellular signal-regulated kinase (ERK) pathway, that regulates cell growth and differentiation is involved. Details of the signal transduction pathway including the ERK, phosphatidylinositide 3-kinase (PI3K) and phosphoinositide phospholipase C-γ (PLCγ) pathway-mediated calcium ion mobilization and cellular events have been illustrated in a review by Numakawa et al. (2010). 0.0% topic match

0.0%

0.0

1988

[418] viewpoint Expression and possible function of nerve growth factor receptors on $chwann cells Eugene M. Johnson and P. Distefano Journal Not Provided 1988 - 0 citations - Show abstract - Cite 0.0% topic match

0.0%

0.0

2007

[419] Neurotrophins and Their Receptors M. Bothwell https://doi.org/10.1002/9780470101001.HCN054 2007 - 0 citations - Show abstract - Cite 0.0% topic match

0.0%

1.1

2005

[420] Neurotrophin survival signaling mechanisms. M. Chao and F. Lee Journal of Alzheimer's disease : JAD 2005 - 22 citations - Show abstract - Cite 0.0% topic match

Research topic

Report

References

Select the format you want to download:

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS

Download Citations

Citation Text

BibTeX

RIS