Undermind Research Topic: I would like to discover papers that investigate the molecular mechanism underlying Hebbian learning, and I am particularly interested in papers involving or exploring hormone-like chemicals such as nerve growth factor.

Research topic

I would like to discover papers that investigate the molecular mechanism underlying Hebbian learning, and I am particularly interested in papers involving or exploring hormone-like chemicals such as nerve growth factor.

Report

Several papers investigate the molecular mechanisms underlying Hebbian learning in the context of nerve growth factor (NGF), with key findings demonstrating NGF's role in modulating synaptic plasticity mechanisms such as long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus and visual cortex [3, 5, 6, 7].

Details:

NGF and LTP/LTD:
- Paper [3] provides direct evidence that NGF converts high-frequency stimulation-induced LTP into LTD in rat visual cortex neurons, highlighting NGF’s role in modulating synaptic plasticity in a Hebbian context.
- Paper [5] shows that NGF inhibits the expression of LTP in hippocampal slices, implicating a modulatory role of NGF in synaptic efficacy, a key aspect of Hebbian learning.
- Paper [6] demonstrates that NGF enhances LTP expression in rat dentate gyrus via tyrosine kinase activation, indicating NGF’s capability to facilitate synaptic strength through intracellular signaling pathways involving ERK.

Signaling Mechanisms:
- Paper [10] reports the activation of the ERK pathway by NGF, modulated by calcium and calmodulin, linking NGF signaling to synaptic plasticity mechanisms relevant to Hebbian learning.
- Paper [12] shows that NGF rapidly induces prolonged acetylcholine release from cultured basal forebrain neurons, emphasizing NGF's neuromodulatory actions through TrkA receptors and calcium signaling, elements crucial for Hebbian plasticity.
NGF’s Role in Synaptic Changes and Memory:
- Paper [4] discusses NGF’s facilitation of hippocampal LTP and enhancement of spatial memory in adult rats, providing evidence that NGF contributes to memory and learning through enhancement of synaptic plasticity.
- Paper [7] confirms the essential role of NGF in hippocampal plasticity and learning, illustrating that NGF augmentation increases LTP while its blockade impairs LTP and memory retention.

Conclusion: The literature search revealed significant insights into how NGF influences molecular mechanisms underlying Hebbian learning. NGF modulates synaptic plasticity through various pathways, including conversion of LTP to LTD, enhancement of LTP, and activation of critical signaling mechanisms like the ERK pathway, all of which contribute to synaptic efficacy and plasticity fundamental to Hebbian learning models [3, 5, 6, 7, 10, 12].

References

Last 5 years

Last 2 years

> 1 citation per year

> 5 citations per year

Topic Match

Cit./Year

Year

Paper

Paper Relevance Summary

99.5%

1.5

1999

[1] 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 99.5% topic match

Shows that NGF's role in synaptic plasticity requires electrical activity. Details how NGF signaling via TrkA receptor interacts with afferent electrical activity. Focuses on the visual cortex, providing a specific context for NGF and plasticity studies.

99.2%

0.0

2004

[2] NGF favors LTD over LTP in layer II-III neurons of rat visual cortex. A. Brancucci, ..., and L. Domenici The Journal of Physiology 2004 - 1 citations - Show abstract - Cite 99.2% topic match

99.0%

0.5

2004

[3] 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 99.0% topic match

Provides empirical evidence on NGF's impact on synaptic plasticity. Shows NGF converts HFS-induced LTP into LTD in rat visual cortex neurons. Directly explores NGF's role in synaptic plasticity, relevant for understanding its molecular mechanisms in Hebbian learning.

98.1%

0.0

2000

[4] 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 98.1% topic match

Demonstrates NGF's role in modulating hippocampal LTP and spatial memory. Shows NGF infusion in adult rats enhances synaptic plasticity and memory acquisition via septal-hippocampal pathways. Relevant as it links NGF to molecular mechanisms of LTP, important for Hebbian learning models.

97.7%

0.6

1993

[5] 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 97.7% topic match

Shows NGF's role in inhibiting LTP expression in hippocampal slices. Finds NGF reduces LTP expression concentration-dependently without altering basal synaptic transmission. Indicates a modulatory role of NGF in learning and memory via high-affinity receptors.

97.5%

1.1

1999

[6] 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 97.5% topic match

Shows NGF's role in modulating LTP via tyrosine kinase activation. Demonstrates NGF enhances glutamate release and calcium influx, contributing to LTP expression in rat dentate gyrus. Uses trk inhibitor tyrphostin AG879 to link NGF-induced ERK phosphorylation and synaptic plasticity, aligning with Hebbian learning mechanisms and NGF pathways.

96.9%

11.8

2009

[7] NGF Is Essential for Hippocampal Plasticity and Learning J. Conner, ..., and M. Tuszynski The Journal of Neuroscience 2009 - 180 citations - Show abstract - Cite - PDF 96.9% topic match

Shows the role of NGF in hippocampal plasticity and learning. Demonstrates NGF augmentation enhances LTP and blocking NGF impairs LTP and memory retention. Focuses on molecular mechanisms of NGF but lacks specific exploration of Hebbian learning pathways.

93.9%

1.3

2012

[8] 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 - PDF 93.9% topic match

Provides evidence for activity-dependent anterograde delivery of NGF and its synaptic effects. Shows NGF transported from hippocampal GABAergic neurons to the medial septum increases synaptic efficacy by modulating GABAA receptors. Relevant to Hebbian learning via NGF's role in synaptic modulation and activity-dependent delivery in the hippocamposeptal system.

93.8%

3.5

1994

[9] Short-term modulation of glutamatergic synapses in adult rat hippocampus by NGF. M. Knipper, ..., and Rylett Rj Neuroreport 1994 - 105 citations - Show abstract - Cite 93.8% topic match

Investigates NGF's effects on glutamatergic synapses in the hippocampus. Demonstrates NGF potentiates glutamate release and postsynaptic potentials, linking to Hebbian-like synaptic modulation. Highlights increased synapsin I phosphorylation, suggesting molecular mechanisms related to Hebbian learning processes.

90.3%

1.9

2000

[10] 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 - PDF 90.3% topic match

Provides evidence on NGF activation of the ERK pathway modulated by Ca²⁺ and calmodulin. Explores the role of NGF interacting with TrkA receptors, leading to increased intracellular calcium levels. Relevant as it links NGF signaling and intracellular calcium, pertinent to molecular mechanisms in Hebbian learning.

86.7%

3.2

2010

[11] 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 - 46 citations - Show abstract - Cite - PDF 86.7% topic match

Shows NGF impact on motoneurons' synaptic composition and firing patterns. Investigates NGF delivered to adult cats' abducens motoneurons, examining synaptic plasticity changes. Relevance: Studies NGF's direct role in synaptic remodeling but lacks explicit Hebbian learning focus.

84.9%

3.0

2001

[12] 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 - PDF 84.9% topic match

Shows NGF-induced activity-dependent prolonged ACh release in cultured basal forebrain neurons. Demonstrates NGF's enhancement of ACh release involves TrkA receptors, Ca²⁺, and voltage-gated Ca²⁺ channels. Provides insights into NGF's neuromodulatory effects, potentially relevant to Hebbian learning mechanisms and synaptic plasticity.

84.4%

2.2

2000

[13] Blocking the NGF-TrkA Interaction Rescues the Developmental Loss of LTP in the Rat Visual Cortex Role of the Cholinergic System Emanuele Pesavento, ..., and L. Domenici Neuron 2000 - 54 citations - Show abstract - Cite - PDF 84.4% topic match

82.9%

1.4

2014

[14] 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 82.9% topic match

76.9%

11.8

2005

[15] Neurotrophin-mediated rapid signaling in the central nervous system: mechanisms and functions. R. Blum and A. Konnerth Physiology 2005 - 234 citations - Show abstract - Cite 76.9% topic match

Highlights rapid neurotrophin signaling impacts on synaptic functions. Demonstrates that neurotrophins like NGF modulate membrane excitability and synaptic plasticity through Trk receptor interaction. Provides insights on the molecular mechanisms relevant to Hebbian learning via neurotrophin-Trk receptor pathways, though specifics on Hebbian mechanisms and NGF focus need further verification.

72.8%

0.4

2003

[16] 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 72.8% topic match

Investigates NGF effects on hippocampal cholinergic deficits and learning impairment. Explores continuous NGF infusion's amelioration of deficits in rats with entorhinal cortex lesions. Focuses more on behavioral recovery and cholinergic activity than on specific molecular mechanisms of Hebbian learning.

72.1%

1.9

1993

[17] 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 72.1% topic match

Shows NGF prevents monocular deprivation effects on neuron size in LGN. NGF prevents neuron shrinkage in deprived LGN laminae, indicating a role in geniculo-cortical pathway plasticity.

70.1%

0.0

2009

[18] 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 70.1% topic match

Investigates NGF-induced neuronal activity changes. Uses cultured rat hippocampal slices and a multielectrode array (MEA) system. Focuses on NGF's neuromodulatory roles, potentially linking to Hebbian mechanisms without explicit molecular pathway details.

67.9%

0.4

1997

[19] 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 67.9% topic match

Provides: An overview of trophic factors in synaptic plasticity and memory. Details: Highlights the role of NGF and neurotrophins in synaptic transmission regulation and neural development. Relevance: Lacks specific focus on Hebbian learning but relevant to NGF’s role in synaptic plasticity.

65.7%

0.5

2002

[20] 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 65.7% topic match

Demonstrates NGF enhances neurotransmitter release in PC12 cells. Provides insights into NGF activating PI3K and MAPK pathways to increase Ca²⁺-responsive secretory vesicles. Specifically examines NGF's molecular role without directly linking to Hebbian learning mechanisms but touches on relevant signaling pathways.

63.3%

10.0

1994

[21] 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 63.3% topic match

Demonstrates the regulation of NGF and BDNF by acetylcholine in the hippocampus. Shows that muscarinic receptor activation upregulates NGF and BDNF mRNA and NGF protein levels, influencing synaptic plasticity. Highlights a feedback loop where NGF and BDNF enhance acetylcholine release, suggesting a mechanism for activity-dependent plasticity.

61.3%

0.2

1999

[22] Focal hippocampal gain of NGF function elicits specific septal cholinergic reorganization. A. Brooks, ..., and H. Federoff Neuroreport 1999 - 6 citations - Show abstract - Cite 61.3% topic match

Shows how NGF influences cholinergic reorganization in hippocampus. Demonstrates focal NGF gain increases cholinergic markers and cell size in the septohippocampal projection. Relevant for NGF's role in neuronal restructuring, but lacks direct Hebbian learning mechanism focus.

59.3%

2.3

2021

[23] Intrahippocampal Adeno-Associated Virus–Mediated Overexpression of Nerve Growth Factor Reverses 192IgG-Saporin–Induced Impairments of Hippocampal Plasticity and Behavior Y. Dobryakova, ..., and A. Bolshakov Frontiers in Neuroscience 2021 - 7 citations - Show abstract - Cite - PDF Abstract: One of the aspects of Alzheimer disease is loss of cholinergic neurons in the basal forebrain, which leads to development of cognitive impairment. Here, we used a model of cholinergic deficit caused by immunotoxin 192IgG-saporin to study possible beneficial effects of adeno-associated virus (AAV)–mediated overexpression of nerve growth factor (NGF) in the hippocampus of rats with cholinergic deficit. Suspension of recombinant AAV carrying control cassette or cassette with NGF was injected into both hippocampi of control rats or rats with cholinergic deficit induced by intraseptal injection of 192IgG-saporin. Analysis of choline acetyltransferase (ChAT) immunostaining showed that NGF overexpression in the hippocampus did not prevent strong loss of ChAT-positive neurons in the septal area caused by the immunotoxin. Induction of cholinergic deficit in the hippocampus led to impairments in Y-maze and beam-walking test but did not affect behavioral indices in the T-maze, open field test, and inhibitory avoidance training. NGF overexpression in the rats with cholinergic deficit restored normal animal behavior in Y-maze and beam-walking test. Recording of field excitatory postsynaptic potentials in vivo in the hippocampal CA1 area showed that induction of cholinergic deficit decreased magnitude of long-term potentiation (LTP) and prevented a decrease in paired-pulse ratio after LTP induction, and NGF overexpression reversed these negative changes in hippocampal synaptic characteristics. The beneficial effect of NGF was not associated with compensatory changes in the number of cells that express NGF receptors TrkA and NGFR in the hippocampus and medial septal area. NGF overexpression also did not prevent a 192IgG-saporin–induced decrease in the activity of acetylcholine esterase in the hippocampus. We conclude that NGF overexpression in the hippocampus under conditions of cholinergic deficit induces beneficial effects which are not related to maintenance of cholinergic function. 59.3% topic match

Investigates NGF's effect on hippocampal plasticity under cholinergic deficit. Shows NGF overexpression reverses synaptic impairments without altering NGF receptor cell counts or acetylcholine esterase activity. Relevant for NGF's role in synaptic plasticity but lacks focus on specific Hebbian learning mechanisms.

59.2%

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 - PDF 59.2% topic match

Shows NGF regulation of nitric oxide synthase activity in the hippocampus. Suggests NGF rapidly affects synaptic activity beyond long-term retrograde signaling. Relevance to Hebbian learning may be indirect; core focus on NGF and nitric oxide interactions.

55.0%

16.9

1991

[25] Interplay between glutamate and gamma-aminobutyric acid transmitter systems in the physiological regulation of brain-derived neurotrophic factor and nerve growth factor synthesis in hippocampal neurons. F. Zafra, ..., and D. Lindholm Proceedings of the National Academy of Sciences of the United States of America 1991 - 558 citations - Show abstract - Cite 55.0% topic match

Shows the regulation of NGF synthesis by neurotransmitter systems. Glutamate and GABA balance control NGF mRNA and protein levels in hippocampal neurons.

51.0%

0.5

1993

[26] 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- 51.0% topic match

Provides insights into the expression and regulation of neurotrophins in the hippocampus. Describes the roles of NGF and related neurotrophic factors in neuronal connectivity and maintenance. Relevant for understanding NGF's general role in neuronal systems but lacks specific focus on Hebbian learning mechanisms.

46.6%

2.3

1999

[27] 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 Abstract: We compared, in 4‐ and 23‐month‐old Fischer‐344 rats, the effects of nerve growth factor (NGF) on basal forebrain cholinergic neurons with behavioral performance in acetylcholine‐dependent memory tasks (recent and reference memory). Noncholinergic monoamine markers in target fields of cholinergic neurons were also investigated. We found that NGF has contrasting effects on recent memory in the two age groups in causing improvement in aged rats and deterioration in young rats. In addition, NGF caused significant increase in the size of cholinergic perikarya in all sectors of the basal nucleus complex (BNC). Higher doses of NGF were required to produce hypertrophy in aged animals, a pattern consistent with a lower sensitivity to NGF of aged cholinergic neurons. Analysis of covariance showed that the behavioral effects of NGF were eliminated after covarying out the hypertrophy of cholinergic perikarya. Therefore, NGF causes hypertrophy of cholinergic perikarya regardless of age, and this neurobiological measure correlates with the effects of NGF on recent memory. Reference memory improved moderately only in old rats. This mild effect covaried with an increase in choline acetyltransferase activity in neocortex. Cortical terminal fields of noradrenergic and serotoninergic pathways were not affected by NGF. Taken together, our results indicate that NGF influences recent memory in an age‐ and transmitter‐specific fashion. We postulate that the direct cause of the effects of NGF on memory is not perikaryal hypertrophy per se but rather an increased density of terminals, which always accompanies perikaryal hypertrophy. Although these results continue to support the use of NGF for the treatment of Alzheimer's disease, they raise questions regarding the therapeutic role of NGF for degeneration of BNC neurons occurring in young age. J. Comp. Neurol. 405:491–507, 1999. © 1999 Wiley‐Liss, Inc. 46.6% topic match

Provides evidence that NGF influences memory via structural changes in cholinergic neurons. Shows NGF increases terminal density, affecting memory, independent of perikaryal hypertrophy. Lacks direct investigation into molecular mechanisms of Hebbian learning; focuses on memory and structural neuron changes.

44.9%

2.1

1994

[28] 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 44.9% topic match

Shows NGF's role in neural plasticity by prolonging sensitivity to monocular deprivation. Implanting anti-NGF producing cells delays synapse consolidation in the visual cortex. Indirectly relevant to Hebbian learning; focuses on NGF's effects on a critical period rather than specific Hebbian mechanisms.

43.1%

6.3

1995

[29] 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 - 188 citations - Show abstract - Cite - PDF 43.1% topic match

Shows TrkA expression in CNS neurons responsive to NGF. Examines TrkA expression in the adult rat brain, revealing novel NGF-responsive neurons. Focuses on neurotrophic roles of NGF without detailing Hebbian learning or synaptic plasticity mechanisms.

40.7%

1.3

2005

[30] 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 - PDF 40.7% topic match

Investigates how NGF affects neural firing specifically in the MS/DB. Shows NGF rapidly increases firing rates in cholinergic neurons via TrkA receptors. Focuses on acute NGF exposure and its effects without explicit link to Hebbian learning.

39.6%

2.2

2000

[31] Nerve growth factor collaborates with myocyte-derived factors to promote development of presynaptic sites in cultured sympathetic neurons. S. T. Lockhart, ..., and S. Birren Journal of neurobiology 2000 - 54 citations - Show abstract - Cite 39.6% topic match

Shows NGF's role in synaptic development in sympathetic neurons. Demonstrates NGF collaborates with myocyte-derived factors to enhance presynaptic site formation and synaptic vesicle growth. Focuses on synaptic development rather than Hebbian learning, missing detailed molecular mechanisms tied to plasticity.

39.5%

1.2

2004

[32] Effects of NGF on acetylcholine, acetyl‐CoA metabolism, and viability of differentiated and non‐differentiated cholinergic neuroblastoma cells A. Szutowicz, ..., and H. Bielarczyk Journal of Neurochemistry 2004 - 25 citations - Show abstract - Cite - PDF 39.5% topic match

Investigates NGF’s effects on cholinergic neuroblastoma cell properties. Examines how NGF influences phenotypic traits and viability, considering both p75NTR and TrkA receptors. Focus on acetylcholine metabolism rather than directly on Hebbian learning mechanisms.

35.8%

43.8

2003

[33] BDNF and activity-dependent synaptic modulation. B. Lu Learning & memory 2003 - 952 citations - Show abstract - Cite - PDF 35.8% topic match

Focuses on BDNF in activity-dependent synaptic modulation. Explores mechanisms for BDNF transcription, transport, and TrkB receptor trafficking related to synaptic plasticity. Lacks specific discussion of NGF and its role in Hebbian learning.

34.6%

2.0

2010

[34] Neurogranin and synaptic plasticity balance Ling Zhong and N. Gerges Communicative & Integrative Biology 2010 - 29 citations - Show abstract - Cite - PDF 34.6% topic match

Shows the role of neurogranin in synaptic plasticity. Demonstrates neurogranin enhances synaptic strength in an activity- and NMDA receptor-dependent manner. Does not specifically explore the role of NGF or hormone-like chemicals in Hebbian learning.

34.4%

2.3

1999

[35] Nerve growth factor increases the synthesis and release of acetylcholine and the expression of vesicular acetylcholine transporter in primary cultured rat embryonic septal cells Hiromi Oosawa, ..., and K. Kawashima Journal of Neuroscience Research 1999 - 59 citations - Show abstract - Cite 34.4% topic match

Shows NGF increases ACh synthesis and release in cholinergic neurons. NGF enhances ACh synthesis, vesicular transport, and release, aiding cholinergic neuron development but not survival. Does not directly address Hebbian learning or synaptic plasticity mechanisms.

33.9%

0.5

2018

[36] 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 33.9% topic match

Investigates NGF's effects on rat hippocampal neurons. Demonstrates NGF increases neurite outgrowth and cell survival, suggesting underlying transcriptional regulation. Focuses on transcriptional changes in immune signaling, less direct connection to Hebbian learning mechanisms.

33.5%

6.4

1999

[37] Signaling mechanisms mediating BDNF modulation of synaptic plasticity in the hippocampus. W. Gottschalk, ..., and B. Lu Learning & memory 1999 - 163 citations - Show abstract - Cite - PDF 33.5% topic match

Investigates BDNF in synaptic plasticity. Characterizes signaling pathways (MAPK, PI3K) in BDNF's modulation of synaptic transmission. Mentions neurotrophin signaling pathways similar to NGF but focuses on BDNF, not directly on NGF or Hebbian learning mechanisms.

31.0%

11.1

1997

[38] 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 - PDF 31.0% topic match

Shows that BDNF enhances phosphorylation of NMDA receptor subunit 1. Indicates a rapid, dose-dependent effect of BDNF via trkB receptors in hippocampal neurons. NGF showed no enhancement of phosphorylation, focusing the study on BDNF. Not directly relevant for NGF in Hebbian learning.

28.9%

16.5

1998

[39] 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 - PDF 28.9% topic match

Shows that brain-derived neurotrophic factor (BDNF) increases NMDA receptor activity. Demonstrates BDNF enhances glutamate-evoked currents, implicating trkB receptor activation and NMDA receptor modulation. Focuses on BDNF, not NGF, relevance to Hebbian learning through synaptic strength enhancement via NMDA receptor efficacy.

28.8%

0.0

2008

[40] 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 28.8% topic match

Focuses on BDNF signaling and hippocampal synaptic plasticity. Highlights neurotrophin role in synaptic transmission and Ca²⁺ homeostasis influencing gene expression. Does not investigate NGF or Hebbian learning specifically, limiting relevance.

28.7%

1.6

2011

[41] Neurogranin phosphorylation fine‐tunes long‐term potentiation Ling Zhong, ..., and N. Gerges European Journal of Neuroscience 2011 - 22 citations - Show abstract - Cite - PDF 28.7% topic match

Shows that neurogranin phosphorylation regulates LTP expression. Indicates neurogranin's role in synaptic transmission and LTP at CA1 hippocampal synapses via phosphorylation by protein kinase C. Focuses on general synaptic plasticity mechanisms, but does not involve NGF or Hebbian learning specifically. Unlikely to meet precise relevance.

27.0%

1.9

1994

[42] 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 27.0% topic match

Shows NGF regulation of brain nitric oxide synthase (NOS) in cholinergic neurons. Demonstrates that NGF induces NOS expression via trkA receptors in basal forebrain, influencing forebrain function. Relevant to NGF’s molecular actions but does not specifically address Hebbian learning mechanisms.

24.7%

0.5

1998

[43] 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 24.7% topic match

Investigates NGF effects on septohippocampal neurons in transgenic mice. Shows elevated NGF levels enhance cholinergic function and neuron survival. Focuses more on developmental impacts, not specifically on Hebbian learning mechanisms.

23.0%

8.3

1990

[44] 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 - PDF 23.0% topic match

22.2%

0.7

1995

[45] Involvement of Nerve Growth Factor in Visual Cortex Plasticity Q. Gu Reviews in the Neurosciences 1995 - 22 citations - Show abstract - Cite 22.2% topic match

22.1%

0.6

1998

[46] Functional expression of TrkA receptors in hippocampal neurons Lani Aibel, ..., and M. Chao Journal of Neuroscience Research 1998 - 16 citations - Show abstract - Cite - PDF 22.1% topic match

21.0%

0.1

2015

[47] 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 - PDF 21.0% topic match

Provides an overview of growth factors in synaptic development. Explores multiple growth factors, including NGF, in synaptic and circuit function. Includes studies on molecular mechanisms of activity-dependent synapse formation, relevant to Hebbian learning.

20.2%

2.1

2005

[48] Selective cholinergic immunolesioning affects synaptic plasticity in developing visual cortex N. Kuczewski, ..., and L. Domenici European Journal of Neuroscience 2005 - 41 citations - Show abstract - Cite 20.2% topic match

20.1%

1.7

1987

[49] 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 20.1% topic match

19.3%

2.8

2013

[50] 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 19.3% topic match

Shows involvement of NT-3 in synaptic plasticity. Describes NT-3's role in inducing synaptic efficacy and MF structural reorganization. Focuses on NT-3 and BDNF, potentially lacking direct NGF relevance.

18.8%

4.7

2010

[51] Learning induces neurotrophin signaling at hippocampal synapses LuluY . Chen, ..., and C. Gall Proceedings of the National Academy of Sciences 2010 - 69 citations - Show abstract - Cite 18.8% topic match

Shows learning-induced TrkB activation at hippocampal synapses. Learning increases synaptic TrkB phosphorylation via NMDA receptor-dependent mechanisms in the hippocampus. Focus on BDNF and TrkB signaling, not NGF, makes it somewhat related.

18.3%

3.4

2012

[52] 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 - PDF 18.3% topic match

17.6%

0.1

2011

[53] 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 17.6% topic match

17.2%

3.0

2009

[54] p75 and TrkA Signaling Regulates Sympathetic Neuronal Firing Patterns via Differential Modulation of Voltage-Gated Currents J. Luther and S. Birren The Journal of Neuroscience 2009 - 47 citations - Show abstract - Cite - PDF 17.2% topic match

Shows how NGF signaling through TrkA and p75 regulates neuronal firing. Details divergent effects on sympathetic neuron firing through TrkA and p75 signaling. Does not directly address Hebbian learning or synaptic plasticity mechanisms; focus is on firing patterns rather than synaptic changes.

15.6%

0.5

2003

[55] 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 15.6% topic match

14.9%

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 Abstract: In addition to a clearly defined role of BDNF (Brain‐derived neurotrophic factor) in cell survival and differentiation, this neurotrophin has recently been implicated in hippocampal plasticity, including LTP. Interestingly, the mossy fiber projection to pyramidal cells in area CA3 of the hippocampus contains the highest concentration of BDNF in the CNS (Danzer and McNamara, 2004). Also, BDNF administration results in CA3 hyperexcitability in response to mossy fiber stimulation (H.E. Scharfman et al. 1996). BDNF dramatically enhances mossy fiber field potentials and LTP in vitro (Jiménez et al 08). In vivo BDNF infusions enhance mossy fiber LTP and result in neurogenesis at the mossy fiber synapse (Gomez‐Palacio‐Schjetnan and M. Escobar et al., 2008). Previous work found that BDNF mRNA is upregulated in the hippocampus following in vivo mossy fiber LTP (Thompson et al. 2003). In this study we addressed the question of whether other neurothrophins such as NT3 and NGF are involved in LTP at the mossy fiber synapse. Using a hippocampal slice preparation, we recorded field potentials at CA3 pyramidal cells following high frequency stimulation (HFS; 2 trains 100 Hz, 1 sec duration) of the mossy fiber pathway, and observed the effects of bath application of BDNF (concentration 200 ng/ml). In addition, we recorded field potentials at CA3 pyramidal cells following HFS of the mossy fiber pathway and observed the effects of micropipette application of NT3 (200ng/ml), a tyrosine kinase C (trkC) activator, and NGF (200ng/ml), a tyrosine kinase A (trkA) activator. We found that BDNF alone resulted in mossy fiber LTP, and this effect was further enhanced if BDNF was bath applied prior to HFS whereas enhancement of LTP was not observed following application of NGF or NT3. Our results indicate that BDNF plays a specific role on synaptic plasticity and LTP at the mossy fiber synapse. 14.9% topic match

Shows neurotrophin-specific enhancements in mossy fibers LTP. Investigates the role of BDNF, NT3, and briefly mentions NGF in hippocampal plasticity. Primarily focuses on BDNF; NGF's role in LTP requires further investigation.

13.3%

2.0

1999

[57] 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 - PDF 13.3% topic match

12.6%

0.9

2000

[58] Enhanced learning in mice parallels vector-mediated nerve growth factor expression in hippocampus. A. Brooks, ..., and H. Federoff Human gene therapy 2000 - 21 citations - Show abstract - Cite 12.6% topic match

11.7%

0.3

1990

[59] 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 11.7% topic match

Investigates NGF's effect on cholinergic activity in the brain. NGF increases choline acetyltransferase activity in septal and hippocampal areas of adult rats. Does not specifically explore Hebbian learning mechanisms or synaptic plasticity linked explicitly to NGF.

11.5%

5.3

1997

[60] 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 - PDF 11.5% topic match

11.5%

3.9

2004

[61] Neurotrophin signaling among neurons and glia during formation of tripartite synapses. S. Elmariah, ..., and R. Balice-Gordon Neuron glia biology 2004 - 78 citations - Show abstract - Cite - PDF 11.5% topic match

11.2%

12.9

1998

[62] 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 - PDF 11.2% topic match

10.5%

8.7

1997

[63] Role of Neurotrophins in Synapse Development and Plasticity B. Lu and A. Figurov Reviews in the Neurosciences 1997 - 243 citations - Show abstract - Cite 10.5% topic match

10.5%

1.6

2002

[64] 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 10.5% topic match

10.3%

1.1

1992

[65] Stimulation of Glutamate Receptors Increases Expression of Brain‐Derived Neurotrophic Factor mRNA in Rat Hippocampus a N. Lindefors, ..., and H. Persson Annals of the New York Academy of Sciences 1992 - 36 citations - Show abstract - Cite 10.3% topic match

10.1%

4.9

1998

[66] 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 10.1% topic match

10.1%

46.8

1995

[67] Long-lasting neurotrophin-induced enhancement of synaptic transmission in the adult hippocampus Hyejin Kang and E. Schuman Science 1995 - 1390 citations - Show abstract - Cite 10.1% topic match

9.4%

0.0

2009

[68] 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 9.4% topic match

8.7%

17.9

2000

[69] The Role of Brain-Derived Neurotrophic Factor Receptors in the Mature Hippocampus: Modulation of Long-Term Potentiation through a Presynaptic Mechanism involving TrkB Baoji Xu, ..., and L. Reichardt The Journal of Neuroscience 2000 - 434 citations - Show abstract - Cite - PDF 8.7% topic match

8.6%

19.0

1993

[70] Bidirectional long-term modification of synaptic effectiveness in the adult and immature hippocampus SM Dudek and MF Bear Journal of Neuroscience 1993 - 595 citations - Show abstract - Cite - PDF 8.6% topic match

8.4%

3.3

1996

[71] 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 8.4% topic match

8.3%

8.1

1992

[72] 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 - PDF Abstract: The hypothesis that NGF could play a role in the plasticity of the developing mammalian visual cortex was tested in monocularly deprived (MD) rats. In particular, we have asked whether an exogenous supply of NGF could prevent the changes in ocular dominance distribution induced by monocular deprivation. Hooded rats were monocularly deprived for 1 month, starting at postnatal day 14 (P14), immediately before eye opening, by means of eyelid suture. In eight rats, only monocular deprivation was performed; in eight rats, monocular deprivation was combined with intraventricular injections of beta-NGF, and in three rats, with intraventricular injections of cytochrome C. Injections (2 microliters) were given every other day for a period of 1 month. Single neuron activity was recorded in the primary visual cortex of MD rats, MD rats treated with NGF, and MD rats treated with cytochrome C at the end of the deprivation period, and in normal rats of the same age. We found that monocular deprivation caused a striking change in the ocular dominance distribution of untreated MD rats, reducing binocular cells by a factor of two and increasing by a factor of eight the number of cells dominated by the nondeprived eye. In MD NGF-treated rats, the ocular dominance distribution was indistinguishable from the normal. Cytochrome C treatment was completely ineffective in preventing the ocular dominance shift induced by monocular deprivation. To test whether NGF affected cortical physiology or interfered with transmission of visual information, we evaluated in NGF-treated rats the spontaneous discharge and the orientation selectivity. We found these functional properties to be in the normal range. We conclude that NGF is effective in preventing the effects of monocular deprivation in the rat visual cortex and suggest that NGF is a crucial factor in the competitive processes leading to the stabilization of functional geniculocortical connections during the critical period. 8.3% topic match

8.3%

5.1

1996

[73] 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 8.3% topic match

8.2%

3.2

1992

[74] 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 - 105 citations - Show abstract - Cite 8.2% topic match

8.0%

None

[75] 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. 8.0% topic match

7.7%

16.2

1997

[76] 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 7.7% topic match

7.6%

7.2

1995

[77] Cholinergic modulation of activity-dependent synaptic plasticity in the piriform cortex and associative memory function in a network biophysical simulation M. Hasselmo and E. Barkai Journal of Neuroscience 1995 - 210 citations - Show abstract - Cite - PDF Abstract: The effect of activation of cholinergic receptors on long-term potentiation (LTP) in rat piriform cortex pyramidal cells was studied using extracellular and intracellular recordings in brain slice preparations. The functional role of this modulation was studied in a realistic network biophysical stimulation. Repetitive stimuli were applied in two paradigms: one in which the recorded cell was held at its resting potential and one in which synaptic activity was superimposed on a depolarizing pulse strong enough to evoke four action potentials. In the absence of cholinergic modulation, stimulation at 5 Hz induced LTP primarily in the second condition (13.7%, n = 6 out of 9, measured at 10 min after tetanus). When stimuli were applied in the presence of the muscarinic agonist carbachol (20 microM), LTP of greater amplitude was induced in both paradigms (resting: 41.5%, n = 11 out of 16, depolarized: 36%, n = 5 out of 7, measured at 10 min after tetanus). Increases in excitatory postsynaptic potential (EPSP) amplitudes in the presence of carbachol were gradual, starting at the time 5 Hz stimuli were applied and continuing until an action potential was evoked synaptically. In the presence of the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (APV), LTP could not be induced. The muscarinic antagonist atropine also prevented LTP induction in the presence of carbachol. Cholinergic modulation of synaptic plasticity was examined in a previously developed realistic biophysical network simulation. In simulations, use of a gradual rate of synaptic modification prevented excessive strengthening of synapses, which could cause interference between stored patterns. The effect of excess synaptic strengthening can be avoided by introducing activity dependent depression of synaptic strength. Coactivation of learning and depression rules results in a stable system where no interference occurs, at any rate of learning. Implementing the depression rule only during recall does not improve the network's performance. This implies that reduction in the strength of synaptic connections should occur in the presence of ACh, more than in normal conditions. We propose that two effects of ACh--enhancement of LTP and enhancement of LTD--should act together to increase the stability of the cortical network in the process of acquiring information. 7.6% topic match

7.6%

5.5

1995

[78] 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 - PDF 7.6% topic match

7.5%

3.6

1994

[79] Highly selective effects of nerve growth factor, brain‐derived neurotrophic factor, and neurotrophin‐3 on intact and injured basal forebrain magnocellular neurons V. Koliatsos, ..., and J. Winslow Journal of Comparative Neurology 1994 - 109 citations - Show abstract - Cite Abstract: Cholinergic neurons of the basal nucleus complex (BNC) respond to nerve growth factor (NCF), the first member of a polypeptide gene family that also includes brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT‐3), and neurotrophin‐4/5 (NT‐4/5), NGF, BDNF, and NT‐3 are enriched in hippocampus. In addition, NGF and, more recently, BDNF have been shown to stimulate the cholinergic differentiation and enhance the survival of BNC cells in vitro. The present investigation was designed to test, in a comparative fashion, the in vivo effects of human recombinant NGF, BDNF, and NT‐3 with confirmed activities in vitro on cholinergic and γ‐aminobutyric acid (GABA)‐ergic BNC neurons. The specific questions asked were whether and, to what extent, biologically active recombinant neurotrophins stimulate the transmitter phenotypes of intact cholinergic and GABAergic neurons of the BNC, and whether, and to what extent, recombinant neurotrophins protect the transmitter phenotypes of axotomized cholinergic and GABAergic neurons of the BNC following complete transections of the fimbria‐fornix (measured by ChAT mRNA hybridization). Our results confirm the profound stimulatory and p75NGFR expression in both intact and axotomized cholinergic neurons and to exert minor effects on some cholinergic markers (e.g., ChAT immunoreactivity). NT‐3 had no influence on GABAergic neurons. Taken together, these results indicate that, despite their significant sequence homologies and their shared abundance in target fields of BNC neurons, NGF, BDNF, and NT‐3 show striking differences in their efficacies as cholinergic trophic factors. GABAergic neurons of the BNC are resistant to neurotrophins. The result of the present investigation establish that NGF excels among neurotrophins as a trophic factor for intact and injured basal forebrain cholinergic neurons. © 1994 Wiley‐Liss, Inc. 7.5% topic match

7.4%

2.9

1999

[80] From visual experience to visual function: roles of neurotrophins. N. Berardi and L. Maffei Journal of neurobiology 1999 - 72 citations - Show abstract - Cite 7.4% topic match

7.3%

1.2

2000

[81] Gene-experience interaction alters the cholinergic septohippocampal pathway of mice. A. Brooks, ..., and H. Federoff Proceedings of the National Academy of Sciences of the United States of America 2000 - 30 citations - Show abstract - Cite - PDF Abstract: Spatial learning requires the septohippocampal pathway. The interaction of learning experience with gene products to modulate the function of a pathway may underlie use-dependent plasticity. The regulated release of nerve growth factor (NGF) from hippocampal cultures and hippocampus, as well as its actions on cholinergic septal neurons, suggest it as a candidate protein to interact with a learning experience. A method was used to evaluate NGF gene-experience interaction on the septohippocampal neural circuitry in mice. The method permits brain region-specific expression of a new gene by using a two-component approach: a virus vector directing expression of cre recombinase; and transgenic mice carrying genomic recombination substrates rendered transcriptionally inactive by a "floxed" stop cassette. Cre recombinase vector delivery into transgenic mouse hippocampus resulted in recombination in 30% of infected cells and the expression of a new gene in those cells. To examine the interaction of the NGF gene and experience, adult mice carrying a NGF transgene with a floxed stop cassette (NGFXAT) received a cre recombinase vector to produce localized unilateral hippocampal NGF gene expression, so-called "activated" mice. Activated and control nonactivated NGFXAT mice were subjected to different experiences: repeated spatial learning, repeated rote performance, or standard vivarium housing. Latency, the time to complete the learning task, declined in the repeated spatial learning groups. The measurement of interaction between NGF gene expression and experience on the septohippocampal circuitry was assessed by counting retrogradely labeled basal forebrain cholinergic neurons projecting to the hippocampal site of NGF gene activation. Comparison of all NGF activated groups revealed a graded effect of experience on the septohippocampal pathway, with the largest change occurring in activated mice provided with repeated learning experience. These data demonstrate that plasticity of the adult spatial learning circuitry can be robustly modulated by experience-dependent interactions with a specific hippocampal gene product. 7.3% topic match

7.2%

0.3

2019

[82] Long-term synaptic plasticity in hippocampal neurogliaform interneurons M. Mercier, ..., and D. Kullmann bioRxiv 2019 - 2 citations - Show abstract - Cite - PDF 7.2% topic match

7.1%

1.2

2003

[83] Modulation of nerve growth factor‐induced activation of MAP kinase in PC12 cells by inhibitors of nitric oxide synthase B. Kalisch, ..., and R. Rylett Journal of Neurochemistry 2003 - 26 citations - Show abstract - Cite 7.1% topic match

7.0%

0.2

1989

[84] Regulation of Synaptic Molecular Architecture in a Rat Sympathetic Ganglion and Hippocampus K. Wu and I. Black Journal of Cognitive Neuroscience 1989 - 6 citations - Show abstract - Cite 7.0% topic match

7.0%

6.7

1993

[85] Cholinergic regulation of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) but not neurotrophin-3 (NT-3) mRNA levels in the developing rat hippocampus Maria, ..., and Lindholml Journal of Neuroscience 1993 - 210 citations - Show abstract - Cite - PDF 7.0% topic match

6.9%

1.0

1999

[86] Long term depression is expressed during postnatal development in rat visual cortex: a role for visual experience. E. Sermasi, ..., and L. Domenici Brain research. Developmental brain research 1999 - 25 citations - Show abstract - Cite 6.9% topic match

6.9%

36.0

1986

[87] Nerve growth factor promotes survival of septal cholinergic neurons after fimbrial transections F. Hefti Journal of Neuroscience 1986 - 1380 citations - Show abstract - Cite - PDF 6.9% topic match

6.9%

34.0

1995

[88] Neurotrophins regulate dendritic growth in developing visual cortex A. McAllister, ..., and L. C. Katz Neuron 1995 - 992 citations - Show abstract - Cite 6.9% topic match

6.6%

19.2

1999

[89] Impairments in High-Frequency Transmission, Synaptic Vesicle Docking, and Synaptic Protein Distribution in the Hippocampus of BDNF Knockout Mice Lucas Pozzo-Miller, ..., and B. Lu The Journal of Neuroscience 1999 - 489 citations - Show abstract - Cite - PDF 6.6% topic match

6.4%

21.5

1995

[90] 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 - 629 citations - Show abstract - Cite - PDF 6.4% topic match

6.4%

32.0

2002

[91] From acquisition to consolidation: on the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning. W. Tyler, ..., and Lucas Pozzo-Miller Learning & memory 2002 - 711 citations - Show abstract - Cite - PDF 6.4% topic match

6.3%

1.2

1993

[92] Neurotropism of Nerve Growth Factor for Adult Rat Septal Cholinergic Axons in Vivo T. Hagg and S. Varon Experimental Neurology 1993 - 39 citations - Show abstract - Cite 6.3% topic match

6.3%

2.7

2005

[93] Regulation of cholinergic gene expression by nerve growth factor depends on the phosphatidylinositol‐3′‐kinase pathway B. Madziar, ..., and B. Berse Journal of Neurochemistry 2005 - 54 citations - Show abstract - Cite - PDF 6.3% topic match

6.2%

0.3

2006

[94] β2-Adrenoceptor Agonist Clenbuterol Causes NGF Expression and Neuroprotection Yuan Zhu and J. Krieglstein Cns Drug Reviews 2006 - 6 citations - Show abstract - Cite Abstract: Neurotrophic factors such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT3), and neurotrophin-4/5 (NT4/5) play an important role in the regulation of nervous system development and adult nervous system plasticity, maintenance of structural integrity, and mediation of defensive responses after CNS injuries. NGF, probably the most widely studied neurotrophic factor, has been found to support both peripheral sympathetic and sensory neurons (17,46,47,65), and to promote the survival of basal forebrain cholinergic neurons (16), which project from the septum-diagonal band and basal nucleus to the hippocampus and cerebral cortex, respectively (25,30). Under physiological conditions, the highest NGF concentration is found in the hippocampus, whereas the basal forebrain contains a low level of NGF, suggesting that NGF is produced in these cholinergic target regions and then retrogradely transported to the cell bodies in the basal forebrain. It has been previously reported that NGF is able to prevent hypoglycemic damage of cultured cortical and hippocampal neurons (8) and glutamate excitotoxicity (67,68). Intraventricular or intrahippocampal administration of NGF can protect rat hippocampus and cortex from ischemic damage (5,27,28,69). Alternatively, Ishimaru et al. (37) showed that NGF infused into the cerebroventricular system delayed rather than prevented neuronal death in the hippocampus after ischemia. The neuroprotective potency of NGF in vivo seems to be correlated with the available amount of NGF and the maintenance of NGF in brain tissue. Thus, it is well-established that NGF possesses a protective function in those brain regions which are particularly vulnerable to cerebral ischemia and chronic neurodegenerative disorders. NGF can be quickly induced in brain tissue in response to seizures, hypoglycemia, or ischemia (24,40). Accordingly, Hellweg et al. (31) proposed a time course of NGF ex- 6.2% topic match

6.1%

4.9

1997

[95] 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 6.1% topic match

6.1%

0.2

1997

[96] 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 … 6.1% topic match

5.9%

3.6

1995

[97] 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 - PDF 5.9% topic match

5.8%

40.5

1996

[98] Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus A. Figurov, ..., and B. Lu Nature 1996 - 1152 citations - Show abstract - Cite 5.8% topic match

5.7%

5.4

1996

[99] The neurotrophic hypothesis: where does it stand? A. Davies Philosophical transactions of the Royal Society of London. Series B, Biological sciences 1996 - 154 citations - Show abstract - Cite Abstract: In the developing peripheral nervous system many neurons die shortly after their axons reach their target fields. This loss is thought to match the number of neurons to the size and requirements of their target fields because altering target field size before innervation affects the number of neurons that survive. The neurotrophic hypothesis provides an explanation for how target fields influence the size of the neuronal populations that innervate them. This hypothesis arose from work on nerve growth factor (NGF), the founder member of the neurotrophin family of secreted proteins. Its principal tenet is that the survival of developing neurons depends on the supply of a neurotrophic factor that is synthesized in limiting amounts in their target fields. The neurotrophic hypothesis has, however, been broadened by the demonstration that multiple neurotrophic factors regulate the survival of certain populations of neurons. For example, some neurons depend on several different neurotrophic factors which may act concurrently or sequentially during target field innervation. In addition, there are aspects of neurotrophin action that do not conform with the classic neurotrophic hypothesis. For example, the dependence of some populations of sensory neurons on particular neurotrophins before significant neuronal death takes place raises the possibility that the supply of these neurotrophins is not limiting for survival at this stage of development. There is also evidence that at stages before and after sensory neurons depend on target-derived neurotrophins for survival, neurotrophins act on at least some sensory neurons by an autocrine route. Yet despite the growing wealth of information on the multiple roles and modes of action of neurotrophic factors, the neurotrophic hypothesis has remained the best explanation for how neuronal target fields in the developing peripheral nervous system regulate their innervation density. 5.7% topic match

5.6%

18.4

1993

[100] Heightened synaptic plasticity of hippocampal CA1 neurons during a Cholinergically induced rhythmic state P. T. Huerta and J. Lisman Nature 1993 - 576 citations - Show abstract - Cite 5.6% topic match

5.5%

0.2

2004

[101] 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 5.5% topic match

5.5%

2.6

2001

[102] 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 - PDF 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. 5.5% topic match

5.5%

2.1

1998

[103] 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 5.5% topic match

5.3%

0.3

1993

[104] TRANS SYNAPTIC CONTROL OF GENE EXPRESSION R. Armstrong and M. Montminy Journal Not Provided 1993 - 8 citations - Show abstract - Cite 5.3% topic match

5.3%

2.3

2000

[105] Intraparenchymal NGF Infusions Rescue Degenerating Cholinergic Neurons M. Tuszynski Cell Transplantation 2000 - 56 citations - Show abstract - Cite - PDF 5.3% topic match

5.1%

66.7

1995

[106] Neurotrophins and Neuronal Plasticity H. Thoenen Science 1995 - 1940 citations - Show abstract - Cite 5.1% topic match

5.1%

0.1

2005

[107] / Calmodulin-Dependent Protein Kinase II — Discovery , Progress in a Quarter of a Century , and Perspective : Implication for Learning and Memory Takashi Journal Not Provided 2005 - 2 citations - Show abstract - Cite Abstract: In the central nervous system (CNS), the synapse is a specialized junctional complex by which axons and dendrites emerging from different neurons intercommunicate. Changes in the efficiency of synaptic transmission are important to a number of aspects of neural function. Synaptic transmission occurs through neurotransmitters. Synaptic plasticity is defined as an activity-dependent change in synaptic transmission. Transient modifications of synapses have been associated with short-term memory and more lasting changes have been associated with long-term memory in the mature neuron. Neurotransmitters and other signaling molecules bind to cell surface receptors, and regulate cellular functions. Signal transduction mechanisms at the plasma membrane lead to the generation of intracellular signals and second messengers. These molecules interact with specific target molecules to initiate a cascade of biochemical events and lead to a change in cellular function. Calcium ion (Ca ) is an universal second messenger in eukaryotic cells. Ca plays an essential role in the basic operation of neurons through synaptic communication. Cells typically maintain an intracellular Ca level of 10 7 M, which is 10 times lower the level outside the cells. The intracellular Ca level rapidly increases up to 10 4 M derived from extracellular and intracellular sources in response to extra cellular stimuli. The predominant intracellular receptor of Ca is calmodulin, a EF-hand family Ca binding protein. Calmodulin is a highly conserved Ca sensor that is ubiquitously expressed in mammalian cells, and its major targets are protein kinases. Protein phosphorylation is a major regulatory mechanism of signal transduction. A large number of extraceluular signalings have been shown to regulate protein phosphorylation in the nervous system. Neuronal CaM kinase II became known as a memory molecule with the report that transgenic mice lacking the a isoform of this kinase are defective in long-term potentiation (LTP, a potential cellular mechanisms of learning and memory) and spatial learning, and interest has been directed foward the molecular mechanism of learning and memory through the action of this kinase. There are many interesting features of this kinase. This review will focus on various aspects of neuronal CaM kinase II. Figure 1 shows a schematic representation of the activation of CaM kinase II and of the regulation of neuronal functions. Several other reviews on CaM kinase II provide additional perspectives for the interested reader. 5.1% topic match

5.1%

1.0

1989

[108] Intracellular Storage and Evoked Release of Acetylcholine from Postnatal Rat Basal Forebrain Cholinergic Neurons in Culture with Nerve Growth Factor N. Takei, ..., and H. Hatanaka Journal of Neurochemistry 1989 - 36 citations - Show abstract - Cite 5.1% topic match

4.8%

0.0

2023

[109] Brain-derived neurotrophic factor signaling in the neuromuscular junction during developmental axonal competition and synapse elimination. J. Tomàs, ..., and M. Lanuza Neural regeneration research 2023 - 0 citations - Show abstract - Cite Abstract: During the development of the nervous system, there is an overproduction of neurons and synapses. Hebbian competition between neighboring nerve endings and synapses performing different activity levels leads to their elimination or strengthening. We have extensively studied the involvement of the brain-derived neurotrophic factor-Tropomyosin-related kinase B receptor neurotrophic retrograde pathway, at the neuromuscular junction, in the axonal development and synapse elimination process versus the synapse consolidation. The purpose of this review is to describe the neurotrophic influence on developmental synapse elimination, in relation to other molecular pathways that we and others have found to regulate this process. In particular, we summarize our published results based on transmitter release analysis and axonal counts to show the different involvement of the presynaptic acetylcholine muscarinic autoreceptors, coupled to downstream serine-threonine protein kinases A and C (PKA and PKC) and voltage-gated calcium channels, at different nerve endings in developmental competition. The dynamic changes that occur simultaneously in several nerve terminals and synapses converge across a postsynaptic site, influence each other, and require careful studies to individualize the mechanisms of specific endings. We describe an activity-dependent balance (related to the extent of transmitter release) between the presynaptic muscarinic subtypes and the neurotrophin-mediated TrkB/p75NTR pathways that can influence the timing and fate of the competitive interactions between the different axon terminals. The downstream displacement of the PKA/PKC activity ratio to lower values, both in competing nerve terminals and at postsynaptic sites, plays a relevant role in controlling the elimination of supernumerary synapses. Finally, calcium entry through L- and P/Q- subtypes of voltage-gated calcium channels (both channels are present, together with the N-type channel in developing nerve terminals) contributes to reduce transmitter release and promote withdrawal of the most unfavorable nerve terminals during elimination (the weakest in acetylcholine release and those that have already become silent). The main findings contribute to a better understanding of punishment-rewarding interactions between nerve endings during development. Identifying the molecular targets and signaling pathways that allow synapse consolidation or withdrawal of synapses in different situations is important for potential therapies in neurodegenerative diseases. 4.8% topic match

4.8%

0.6

1998

[110] 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 - PDF 4.8% topic match

4.7%

6.8

2006

[111] 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 - PDF 4.7% topic match

4.6%

9.0

1995

[112] Neurotrophic factors and synaptic plasticity D. Lo Neuron 1995 - 261 citations - Show abstract - Cite 4.6% topic match

4.6%

8.7

1979

[113] Nerve growth factor (NGF) in the rat CNS: Absence of specific retrograde axonal transport and tyrosine hydroxylase induction in locus coeruleus and substantia nigra Martin E. Schwab, ..., and Hans Thoenen Brain Research 1979 - 395 citations - Show abstract - Cite 4.6% topic match

4.4%

2.1

1995

[114] Elementary forms of synaptic plasticity in the visual cortex. A. Kirkwood and M. Bear Biological research 1995 - 63 citations - Show abstract - Cite 4.4% topic match

4.4%

0.1

1988

[115] NERVE GROWTH FACTOR EFFECTS ON eNS NEURONS AND ON BEHAVIORAL RECOVERY FROM BRAIN DAMAGE B. Will, ..., and G. Toniolo Journal Not Provided 1988 - 4 citations - Show abstract - Cite 4.4% topic match

4.4%

10.8

1999

[116] Neurotrophins and hippocampal synaptic transmission and plasticity B. Lu and A. Chow Journal of Neuroscience Research 1999 - 272 citations - Show abstract - Cite 4.4% topic match

4.3%

3.8

2018

[117] Basal forebrain septal nuclei are enlarged in healthy subjects prior to the development of Alzheimer's disease T. Butler, ..., and M. Leon Neurobiology of Aging 2018 - 25 citations - Show abstract - Cite - PDF 4.3% topic match

4.3%

None

[118] 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 … 4.3% topic match

4.2%

0.2

2016

[119] Molecular mechanisms of synaptic plasticity Hongik Hwang Journal Not Provided 2016 - 2 citations - Show abstract - Cite Abstract: Synaptic plasticity serves as a central molecular mechanism underlying learning and memory formation in the brain. An increase in intracellular calcium concentrations triggered by neuronal activity induces synaptic plasticity, and calmodulin is a key protein that detects the elevated calcium levels and propagates downstream signaling. Neurogranin is a neuron-specific protein that binds to calmodulin and regulates the availability of calmodulin in the postsynaptic compartments of excitatory neurons. Dysregulation of neurogranin has been reported to cause altered synaptic plasticity as well as impairment in hippocampus-dependent learning, and is also associated with the higher risk of developing neurodegenerative and psychiatric diseases. Therefore, it is critical to understand how neurogranin regulates the induction of synaptic plasticity in the brain at the molecular level. The focus of this thesis is to examine how the changes in neurogranin expression levels contribute to the induction of synaptic plasticity in the hippocampus with a spike-timing-dependent plasticity paradigm and to understand the underlying molecular mechanisms. Using lentivirus-mediated manipulations of neurogranin levels in hippocampal CAl neurons, we found that increasing neurogranin levels in CAI neurons prolongs the timing window for spike-timing-dependent long-term potentiation (LTP), whereas acute knockdown of neurogranin inhibits the expression of LTP via regulating PP2B activity. We have also found that neurogranin interferes with calcium-dependent inactivation of neuronal Ltype calcium channels and allows a sustained influx of calcium during the membrane depolarization in hippocampal neurons. Our results indicate that dynamic changes in neurogranin levels play a crucial role in setting the threshold for inducing LTP in spike-timing-dependent plasticity in the hippocampus. Thesis Supervisor: Weifeng Xu Title: Assistant Professor ofNeuroscience 4.2% topic match

4.1%

8.3

2005

[120] BDNF regulates primary dendrite formation in cortical neurons via the PI3-kinase and MAP kinase signaling pathways. P. Dijkhuizen and Anirvan Ghosh Journal of neurobiology 2005 - 164 citations - Show abstract - Cite 4.1% topic match

4.0%

1.2

1997

[121] 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. 4.0% topic match

4.0%

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. 4.0% topic match

4.0%

18.4

1992

[123] 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 4.0% topic match

3.9%

3.0

1998

[124] Somatosensory Cortical Plasticity Role of the Basal Forebrain Cholinergic Projection in R. Sachdev, ..., and Ford F. Ebner Journal Not Provided 1998 - 82 citations - Show abstract - Cite 3.9% topic match

3.8%

1.5

2002

[125] 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 - PDF 3.8% topic match

3.6%

2.0

1999

[126] Functional Blockade of Tyrosine Kinase A in the Rat Basal Forebrain by a Novel Antagonistic Anti-Receptor Monoclonal Antibody A. Cattaneo, ..., and M. Novák The Journal of Neuroscience 1999 - 50 citations - Show abstract - Cite - PDF 3.6% topic match

3.6%

0.0

1988

[127] 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 3.6% topic match

3.6%

23.9

2020

[128] The role of cytokines in modulating learning and memory and brain plasticity J. Bourgognon and J. Cavanagh Brain and Neuroscience Advances 2020 - 117 citations - Show abstract - Cite - PDF 3.6% topic match

3.5%

1.5

1999

[129] 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 - PDF 3.5% topic match

3.5%

6.5

2004

[130] Endothelin-1 regulates cardiac sympathetic innervation in the rodent heart by controlling nerve growth factor expression. M. Ieda, ..., and S. Ogawa The Journal of clinical investigation 2004 - 135 citations - Show abstract - Cite - PDF 3.5% topic match

3.5%

5.1

2006

[131] Role of the Neurogranin Concentrated in Spines in the Induction of Long-Term Potentiation A. Zhabotinsky, ..., and J. Lisman The Journal of Neuroscience 2006 - 94 citations - Show abstract - Cite - PDF 3.5% topic match

3.5%

1.1

2002

[132] Inhibitors of nitric oxide synthase attenuate nerve growth factor‐mediated increases in choline acetyltransferase expression in PC12 cells B. Kalisch, ..., and R. Rylett Journal of Neurochemistry 2002 - 25 citations - Show abstract - Cite 3.5% topic match

3.3%

3.1

1989

[133] Effect of anticholinergic drug on long-term potentiation in rat hippocampal slices I. Hirotsu, ..., and T. Ishihara Brain Research 1989 - 112 citations - Show abstract - Cite 3.3% topic match

3.3%

4.5

2000

[134] 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 3.3% topic match

3.3%

0.3

2002

[135] Rat visual cortical neurones express TrkA NGF receptor D. Tropea, ..., and A. Cattaneo Neuroreport 2002 - 7 citations - Show abstract - Cite 3.3% topic match

3.1%

0.9

1992

[136] Effects of nerve growth factor on cortical and striatal acetylcholine and dopamine release in rats with cortical devascularizing lesions D. Maysinger, ..., and A. Cuello Brain Research 1992 - 29 citations - Show abstract - Cite 3.1% topic match

3.0%

0.0

2004

[137] 14 Synaptic Growth, Synaptic Maintenance, and the Persistence of Long-term Memory Storage C. H. Bailey, ..., and E. Kandel https://doi.org/10.1101/087969672.42.431 2004 - 0 citations - Show abstract - Cite 3.0% topic match

3.0%

2.9

2020

[138] Neurogranin Regulates Metaplasticity Ling Zhong and N. Gerges Frontiers in Molecular Neuroscience 2020 - 14 citations - Show abstract - Cite - PDF 3.0% topic match

3.0%

31.2

2003

[139] Neurotrophin secretion: current facts and future prospects V. Lessmann, ..., and M. Malcangio Progress in Neurobiology 2003 - 676 citations - Show abstract - Cite 3.0% topic match

2.9%

11.1

2019

[140] The Importance of Maternal Folate Status for Brain Development and Function of Offspring. E. Naninck, ..., and E. Brouwer-Brolsma Advances in nutrition 2019 - 62 citations - Show abstract - Cite - PDF 2.9% topic match

2.8%

2.8

1994

[141] 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 - PDF 2.8% topic match

2.8%

5.9

2004

[142] Acetylcholine and olfactory perceptual learning. D. Wilson, ..., and R. Sullivan Learning & memory 2004 - 123 citations - Show abstract - Cite - PDF 2.8% topic match

2.8%

3.8

2001

[143] 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 2.8% topic match

2.7%

7.6

1999

[144] Trophic regulation of synaptic plasticity. I. Black Journal of neurobiology 1999 - 191 citations - Show abstract - Cite 2.7% topic match

2.6%

16.4

2004

[145] Regulation of late-phase LTP and long-term memory in normal and aging hippocampus: role of secreted proteins tPA and BDNF Petti T. Pang and B. Lu Ageing Research Reviews 2004 - 328 citations - Show abstract - Cite - PDF 2.6% topic match

2.6%

2.3

2000

[146] 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 2.6% topic match

2.5%

0.1

1994

[147] 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 2.5% topic match

2.4%

12.9

1992

[148] Regulation of brain-derived neurotrophic factor and nerve growth factor mRNA in primary cultures of hippocampal neurons and astrocytes F. Zafra, ..., and H. Thoenen Journal of Neuroscience 1992 - 414 citations - Show abstract - Cite - PDF 2.4% topic match

2.4%

66.5

1982

[149] Theory for the development of neuron selectivity: orientation specificity and binocular interaction in visual cortex E. Bienenstock, ..., and P. Munro Journal of Neuroscience 1982 - 2850 citations - Show abstract - Cite - PDF 2.4% topic match

2.4%

0.9

1987

[150] 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 2.4% topic match

2.4%

0.4

1991

[151] Coordination of trophic interactions by separate developmental programs in sensory neurons and their target fields A. Davies, ..., and K. Vogel Journal of Cell Science 1991 - 13 citations - Show abstract - Cite - PDF 2.4% topic match

2.2%

0.0

1994

[152] Monoclonal antibodies tonervegrowthfactor affect thepostnatal development ofthevisual system N. Berardi, ..., and L. Maffei Journal Not Provided 1994 - 0 citations - Show abstract - Cite 2.2% topic match

2.2%

1.1

1995

[153] 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 - PDF 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. 2.2% topic match

2.1%

2.4

2005

[154] BDNF enhancement of postsynaptic NMDA receptors is blocked by ethanol J. E. Kolb, ..., and E. Levine Synapse 2005 - 47 citations - Show abstract - Cite 2.1% topic match

2.1%

0.0

1994

[155] Platelet-activating factor is the latest candidate retrograde messenger involved in transmitting a signal from the postsynaptic to the presynaptic cell during long-term potentiation. Y. Goda and Long-Term Potentiation Journal Not Provided 1994 - 0 citations - Show abstract - Cite Abstract: Understanding such apparently complex processes as learning and memory may seem a formidable task, but the neuronal signalling systems involved in these processes are likely to share basic components with other, more tractable physiological processes. This is exemplified by the phenomenon known as long-term potentiation (LTP). Brain cells communicate with each other through specialized cell-to-cell contact points known as synaptic terminals. At a synapse, the exocytotic release of signalling molecules from the presynaptic terminal is coupled to a postsynaptic response. LTP refers to the strengthening of this synaptic transmission that is manifested as a long-lasting increase in the postsynaptic response, and is thought by many to be a cellular correlate of memory. LTP can be divided into at least two steps: first, induction, the process by which LTP is triggered; and second, maintenance, the process by which a synapse is altered to increase its efficiency during LTP [1]. Four different intercellular signalling molecules have been implicated as the intercellular messenger molecule involved in the maintenance of LTP: the fatty acid arachidonic acid; nitric oxide (NO), originally identified as 'endothelium-derived relaxing factor', which causes dilation of blood vessels; carbon monoxide (CO); and platelet-activating factor (PAF). LTP occurs at synapses that use glutamate as the transmitter, and is induced by Ca 2+ influx through the NMDA subclass of postsynaptic glutamate receptors, socalled because of its selectivity for the glutamate analog, N-methyl-D-aspartate. Although the induction of LT' has been clearly shown to take place at the postsynaptic cell, the site of maintenance of LTP has been the subject of much controversy. The enhancement of synaptic strength may be maintained by increased transmitter release at the presynaptic terminal, or alternatively, by increased sensitivity of the postsynaptic receptors to released glutamate. Most researchers now agree that both presynaptic and postsynaptic mechanisms are involved in the maintenance of LTP [1i. As LTP is triggered postsynaptically, the existence of a presynaptic mechanism requires a retrograde signal to be sent to the presynaptic terminal (Fig. 1). This is where our candidate retrograde messengers come into play. 2.1% topic match

2.1%

2.9

2001

[156] Mismatch between BDNF mRNA and protein expression in the developing visual cortex: the role of visual experience D. Tropea, ..., and L. Domenici European Journal of Neuroscience 2001 - 68 citations - Show abstract - Cite 2.1% topic match

2.1%

0.4

2002

[157] 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 2.1% topic match

2.0%

32.3

2017

[158] Neurobiology of local and intercellular BDNF signaling Manju Sasi, ..., and R. Blum Pflugers Archiv 2017 - 249 citations - Show abstract - Cite - PDF 2.0% topic match

2.0%

22.2

2002

[159] Mechanism of TrkB-Mediated Hippocampal Long-Term Potentiation L. Minichiello, ..., and M. Korte Neuron 2002 - 492 citations - Show abstract - Cite - PDF 2.0% topic match

2.0%

8.1

2004

[160] Endogenous acetylcholine lowers the threshold for long‐term potentiation induction in the CA1 area through muscarinic receptor activation: in vivo study S. Ovsepian, ..., and M. Rowan European Journal of Neuroscience 2004 - 163 citations - Show abstract - Cite 2.0% topic match

1.9%

10.0

1997

[161] 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 - PDF 1.9% topic match

1.7%

4.3

1996

[162] The action of neurotrophins in the development and plasticity of the visual cortex A. Cellerino and L. Maffei Progress in Neurobiology 1996 - 123 citations - Show abstract - Cite 1.7% topic match

1.7%

2.2

1991

[163] 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 - 71 citations - Show abstract - Cite 1.7% topic match

1.7%

1.1

1995

[164] Axonal regeneration and limited functional recovery following hippocampal deafferentation K. Eagle, ..., and F. Gage Journal of Comparative Neurology 1995 - 31 citations - Show abstract - Cite 1.7% topic match

1.7%

0.9

1996

[165] Participation of nerve growth factor in the regulation of ovarian function G. Dissen, ..., and S. Ojeda Zygote 1996 - 26 citations - Show abstract - Cite 1.7% topic match

1.7%

2.9

1988

[166] 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 1.7% topic match

1.7%

1.6

1993

[167] 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 - PDF 1.7% topic match

1.6%

0.6

2010

[168] Glial cell line-derived neurotrophic factor (GDNF) enhances sympathetic neurite growth in rat hearts at early developmental stages. K. Miwa, ..., and I. Kodama Biomedical research 2010 - 8 citations - Show abstract - Cite - PDF 1.6% topic match

1.6%

0.2

2020

[169] The Mixture of Gotu Kola, Cnidium Fruit, and Goji Berry Enhances Memory Functions by Inducing Nerve-Growth-Factor-Mediated Actions Both In Vitro and In Vivo J. Choi, ..., and S. Kim Nutrients 2020 - 1 citations - Show abstract - Cite - PDF 1.6% topic match

1.6%

0.6

2014

[170] Spatial gene's (Tbata) implication in neurite outgrowth and dendrite patterning in hippocampal neurons Miriam Yammine, ..., and C. Nguyen Molecular and Cellular Neuroscience 2014 - 6 citations - Show abstract - Cite 1.6% topic match

1.5%

8.8

2019

[171] Selective decline of neurotrophin and neurotrophin receptor genes within CA1 pyramidal neurons and hippocampus proper: Correlation with cognitive performance and neuropathology in mild cognitive impairment and Alzheimer's disease S. Ginsberg, ..., and E. Mufson Hippocampus 2019 - 49 citations - Show abstract - Cite - PDF Abstract: Hippocampal CA1 pyramidal neurons, a major component of the medial temporal lobe memory circuit, are selectively vulnerable during the progression of Alzheimer's disease (AD). The cellular mechanism(s) underlying degeneration of these neurons and the relationship to cognitive performance remains largely undefined. Here, we profiled neurotrophin and neurotrophin receptor gene expression within microdissected CA1 neurons along with regional hippocampal dissections from subjects who died with a clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI), or AD using laser capture microdissection (LCM), custom‐designed microarray analysis, and qPCR of CA1 subregional dissections. Gene expression levels were correlated with cognitive test scores and AD neuropathology criteria. We found a significant downregulation of several neurotrophin genes (e.g., Gdnf, Ngfb, and Ntf4) in CA1 pyramidal neurons in MCI compared to NCI and AD subjects. In addition, the neurotrophin receptor transcripts TrkB and TrkC were decreased in MCI and AD compared to NCI. Regional hippocampal dissections also revealed select neurotrophic gene dysfunction providing evidence for vulnerability within the hippocampus proper during the progression of dementia. Downregulation of several neurotrophins of the NGF family and cognate neurotrophin receptor (TrkA, TrkB, and TrkC) genes correlated with antemortem cognitive measures including the Mini‐Mental State Exam (MMSE), a composite global cognitive score (GCS), and Episodic, Semantic, and Working Memory, Perceptual Speed, and Visuospatial domains. Significant correlations were found between select neurotrophic expression downregulation and neuritic plaques (NPs) and neurofibrillary tangles (NFTs), but not diffuse plaques (DPs). These data suggest that dysfunction of neurotrophin signaling complexes have profound negative sequelae within vulnerable hippocampal cell types, which play a role in mnemonic and executive dysfunction during the progression of AD. 1.5% topic match

1.4%

3.9

2021

[172] Pleiotropic activity of nerve growth factor in regulating cardiac functions and counteracting pathogenesis E. Pius-Sadowska and B. Machaliński ESC Heart Failure 2021 - 15 citations - Show abstract - Cite - PDF 1.4% topic match

1.4%

44.3

2010

[173] Postsynaptic BDNF‐TrkB signaling in synapse maturation, plasticity, and disease Akira Yoshii and M. Constantine‐Paton Developmental Neurobiology 2010 - 656 citations - Show abstract - Cite 1.4% topic match

1.3%

11.0

1995

[174] Characterization of Nerve Growth Factor (NGF) Release from Hippocampal Neurons: Evidence for a Constitutive and an Unconventional Sodium‐dependent Regulated Pathway Andreas Blochl and H. Thoenen European Journal of Neuroscience 1995 - 323 citations - Show abstract - Cite 1.3% topic match

1.3%

2.2

1987

[175] Nerve growth factor increases the number of functional Na channels and induces TTX-resistant Na channels in PC12 pheochromocytoma cells B. Rudy, ..., and L. Greene Journal of Neuroscience 1987 - 81 citations - Show abstract - Cite - PDF 1.3% topic match

1.3%

1.0

1996

[176] Differential Effects of Nerve Growth Factor on Expression of Choline Acetyltransferase and Sodium‐Coupled Choline Transport in Basal Forebrain Cholinergic Neurons in Culture J. Pongrac and R. Rylett Journal of Neurochemistry 1996 - 29 citations - Show abstract - Cite 1.3% topic match

1.3%

3.0

2008

[177] 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 - PDF 1.3% topic match

1.3%

5.4

1990

[178] Muscarinic receptor activation facilitates the induction of long-term potentiation (LTP) in the rat dentate gyrus E. Burgard and J. Sarvey Neuroscience Letters 1990 - 186 citations - Show abstract - Cite 1.3% topic match

1.3%

24.7

1993

[179] The neurotrophic factor concept: a reexamination S. Korsching Journal of Neuroscience 1993 - 775 citations - Show abstract - Cite - PDF Abstract: The neurotrophic factor concept in its basic form envisages that innervated tissues produce a signal for the innervating neurons for the selective limitation of neuronal death occurring during development (Purves, 1986; Oppenheim, 1991). This concept arose several decades ago on the basis of the observation that experimental manipulation of the amount of target tissue could modulate the size of neuronal populations. By making the survival of neurons dependent on their target, nature would provide a means to match neuron and target cell populations. NGF, discovered in the 1950s, represents the first known molecular realization of the neurotrophic factor concept. NGF was found to regulate survival, neurite growth, and neurotransmitter production of a particular neuronal type, the sympathetic neurons of the PNS. NGF produced by target cells is specifically bound and internalized by sympathetic neurons, followed by retrograde axonal transport of NGF to the cell soma, where NGF exerts its effects via the cotransported receptor molecule (Levi-Montalcini, 1987; Thoenen et al., 1987). Strictly speaking, increased neurite growth and neurotransmitter production are not trophic effects; however, I will use the term “neurotrophic” in the extended meaning of enhancing neuronal differentiation as well as neuronal survival. It was expected that these results could be generalized to a model of multiple, mutually independent, retrograde trophic messengers, which are synthesized in distinct target areas and act on restricted neuronal types (Fig. 1). This assumption leads to a conceptually simple way to arrange and maintain a variety of neuronal subsystems. One might call this a modular approach to the construction of the nervous system. The hypothesis of multiple retrograde signals has gained widespread experimental support in recent years. Originally proposed for the PNS, the model could be extended to the CNS, in which target neurons synthesize trophic factors for their afferent neurons (Ernfors et al., 1990b). In addition to NGF, a family of NGF-related molecules (now commonly called neurotrophins), which are thought to exert retrograde trophic influences (DiStefano et al., 1992), has been identified. 1.3% topic match

1.3%

0.3

1987

[180] Effect of injury on nerve growth factor uptake by sensory ganglia T. Khan, ..., and J. Perez-Polo Journal of Neuroscience Research 1987 - 10 citations - Show abstract - Cite 1.3% topic match

1.3%

6.9

2023

[181] Post-stroke cognitive impairment and synaptic plasticity: A review about the mechanisms and Chinese herbal drugs strategies Xiansu Chi, ..., and Wei Shen Frontiers in Neuroscience 2023 - 12 citations - Show abstract - Cite - PDF 1.3% topic match

1.2%

4.9

1995

[182] Overexpression of NGF within the heart of transgenic mice causes hyperinnervation, cardiac enlargement, and hyperplasia of ectopic cells. Alborz Hassankhani, ..., and H. Federoff Developmental biology 1995 - 145 citations - Show abstract - Cite 1.2% topic match

1.1%

1.0

1994

[183] 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 1.1% topic match

1.1%

2.2

1996

[184] Selective Effects of Nerve Growth Factor on Spatial Recent Memory as Assessed by a Delayed Nonmatching-to-Position Task in the Water Maze A. Markowska, ..., and V. Koliatsos The Journal of Neuroscience 1996 - 62 citations - Show abstract - Cite - PDF 1.1% topic match

1.0%

0.3

1999

[185] 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 1.0% topic match

1.0%

0.0

2020

[186] Regulation of anterograde transcytosis of neurotrophin receptors and its role in health and diseases N. Yamashita Proceedings for Annual Meeting of The Japanese Pharmacological Society 2020 - 0 citations - Show abstract - Cite - PDF 1.0% topic match

1.0%

1.0

2018

[187] Targeted Mutation (R100W) of the Gene Encoding NGF Leads to Deficits in the Peripheral Sensory Nervous System Wanlin Yang, ..., and Chengbiao Wu Frontiers in Aging Neuroscience 2018 - 6 citations - Show abstract - Cite - PDF 1.0% topic match

0.9%

22.3

2003

[188] Selectivity in neurotrophin signaling: theme and variations. R. Segal Annual review of neuroscience 2003 - 467 citations - Show abstract - Cite 0.9% topic match

0.8%

0.0

1991

[189] Interplay between glutamate andy-aminobutyric acidtransmitter systems inthephysiological regulation ofbrain-derived neurotrophic factor andnervegrowthfactor synthesis in hippocampal neurons F. Zafra Journal Not Provided 1991 - 1 citations - Show abstract - Cite 0.8% topic match

0.8%

33.7

2018

[190] Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases T. Numakawa, ..., and N. Adachi International Journal of Molecular Sciences 2018 - 204 citations - Show abstract - Cite - PDF 0.8% topic match

0.8%

1.5

2006

[191] Nerve growth factor decreases potassium currents and alters repetitive firing in rat sympathetic neurons. J. Luther and S. Birren Journal of neurophysiology 2006 - 28 citations - Show abstract - Cite 0.8% topic match

0.8%

0.2

1987

[192] Denervation‐induced Enhancement of Graft Survival and Growth F. Gage and A. Björklund Annals of the New York Academy of Sciences 1987 - 9 citations - Show abstract - Cite Abstract: Peripheral ganglionic aminergic neurons and spinal cord motoneurons depend on the presence of peripheral target tissue for differentiation and maturation.’-’ The mechanisms regulating this response are not known. One proposal, however, is that the target tissue releases diffusible trophic factors that influence developing neurons. For both ganglionic autonomic neurons and spinal motoneurons, it has been proposed that the survival, differentiation, and axonal outgrowth of axons during development are dependent upon the retrograde transport of trophic factors produced by the target tissue.c9 In the adult rat, if some of the axons supplying a peripheral target tissue are experimentally interrupted, nerve processes from the remaining nerves “sprout ” and reinnervate the denervated target.” In this situation as well, it has been postulated that the denervated target tissue releases a diffusible sprouting stimulus. ’c-” Trophic factors that regulate neuronal survival and differentiation are also probably controlling brain development and regeneration. The existence of neurotrophic factors in the central nervous system (CNS) has been postulated, but, until recently, such factors had only been identified in peripheral tissues. ‘ & I 8 More recently, however, factors with neurotrophic properties have been identified in CNS extracts and wound fluids.’9-2s In fact, nerve growth factor (NGF) has been identified in the CNS.26 It has been postulated that, after damage to the brain, some or all of the neurotrophic factors are available to induce a sprouting response. Several recent experiments support the possibility that diffusible trophic factors are released from the damaged brain and that they assist the survival of embryonic neurons grafted to the brain.20*23-2s In this paper we will review several experiments using the same model system; these experiments strongly suggest that the denervated hippocampal formation (HF) releases several trophic factors, one of which is sufficiently similar to NGF to mimic 0.8% topic match

0.8%

5.9

2004

[193] Rapid BDNF-induced retrograde synaptic modification in a developing retinotectal system Jiu-Lin Du and M. Poo Nature 2004 - 121 citations - Show abstract - Cite 0.8% topic match

0.7%

7.6

1990

[194] Survival of adult basal forebrain cholinergic neurons after loss of target neurons. M. Sofroniew, ..., and Clive N. Svendsen Science 1990 - 264 citations - Show abstract - Cite 0.7% topic match

0.6%

5.8

1995

[195] A single pulse of nerve growth factor triggers long-term neuronal excitability through sodium channel gene induction J. Toledo-Aral, ..., and G. Mandel Neuron 1995 - 173 citations - Show abstract - Cite 0.6% topic match

0.6%

68.9

1996

[196] Physiology of the neurotrophins. G. Lewin and Y. Barde Annual review of neuroscience 1996 - 1991 citations - Show abstract - Cite 0.6% topic match

0.6%

356.8

1993

[197] A synaptic model of memory: long-term potentiation in the hippocampus T. Bliss and G. Collingridge Nature 1993 - 11373 citations - Show abstract - Cite 0.6% topic match

0.6%

3.5

2001

[198] 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 0.6% topic match

0.6%

5.6

1994

[199] A novel cholinergic induction of long-term potentiation in rat hippocampus. J. Auerbach and M. Segal Journal of neurophysiology 1994 - 169 citations - Show abstract - Cite 0.6% topic match

0.5%

10.9

1986

[200] Nerve growth factor gene expression in the developing rat brain. T. Large, ..., and L. Reichardt Science 1986 - 417 citations - Show abstract - Cite 0.5% topic match

0.5%

8.4

1992

[201] Agonists of cholinergic and noradrenergic receptors facilitate synergistically the induction of long-term potentiation in slices of rat visual cortex S. Bröcher, ..., and W. Singer Brain Research 1992 - 274 citations - Show abstract - Cite 0.5% topic match

0.5%

0.8

1999

[202] A new form of synaptic plasticity is transiently expressed in the developing rat visual cortex: a modulatory role for visual experience and brain-derived neurotrophic factor E. Sermasi, ..., and L. Domenici Neuroscience 1999 - 20 citations - Show abstract - Cite 0.5% topic match

0.4%

10.7

1994

[203] TrkA‐immunoreactive profiles in the central nervous system: Colocalization with neurons containing p75 nerve growth factor receptor, choline acetyltransferase, and serotonin T. Sobreviela, ..., and E. Mufson Journal of Comparative Neurology 1994 - 321 citations - Show abstract - Cite - PDF Abstract: The present investigation used an antibody directed against the extracellular domain of the signal transducing nerve growth factor recepto, trkA, to reveal immunoreactive perikarya or fibers within the olfactory bulb and tubercle, cingulate cortex, nucleus accumbens, striatum, endopiriform nucleus, septal/diagonal band complex, nucleus basalis, hippocampal complex, thalamic paraventricular and reuniens nuclei, periventricular hypothalamus, interpeduncular nucleus, mesencephalic nucleus of the fifth nerve, dorsal nucleus of the lateral lemniscus, prepositus hypoglossal nucleus, ventral cochlear nucleus, ventral lateral tegmentum, medial vestibular nucleus, spinal trigeminal nucleus oralis, nucleus of the solitary tract, raphe nuclei, and spinal cord. Colocalization experiments revealed that virtually all striatal trk‐Aimmunoreactive neurons (> 99%) coexpressed choline acetyltransferase (ChAT) but not p75 nerve growth factor receptor (NGFR). Within the septal/diagonal band complex virtually all trkA neurons (> 95%) coexpressed both ChAT and p75 NGFR. More caudally, dual stained sections revealed numerous trkA/ChAT (> 80%) and trkA/p75 NGFR (> 95%) immunoreactive neurons within the nucleus basalis. In the brainstem, raphe serotonergic neurons (45%) coexpressed trkA. Sections stained with a pan‐trk antibody that recognizes primarily trkA, as well as trkB and trkC, labeled neurons within all of these regions as well as within the hypothalamic arcuate, supramammilary, and supraoptic nuclei, hippocampus, inferior and superior colliculus, substantia nigra, ventral tegmental area of T'sai, and cerebellar Purkinje cells. Virtually all of these other regions with the exception of the cerebellum also expressed pan‐trk immunoreactivity in the monkey. The widespread expression of trkA throughout the central neural axis suggests that this receptor may play a role in signal transduction mechanisms linked to NGF‐related substances in cholinergic basal forebrain and noncholinergic systems. These findings suggest that pharmacological use of ligands for trkA could have beneficial effects on the multiple neuronal systems that are affected in such disorders as Alzheimer's disease. © 1994 Wiley‐Liss, Inc. 0.4% topic match

0.4%

29.3

1993

[204] NMDA-receptor-dependent synaptic plasticity: multiple forms and mechanisms R. Malenka and R. Nicoll Trends in Neurosciences 1993 - 909 citations - Show abstract - Cite 0.4% topic match

0.3%

15.1

2013

[205] Death of developing neurons: New insights and implications for connectivity M. Dekkers, ..., and Y. Barde The Journal of Cell Biology 2013 - 167 citations - Show abstract - Cite - PDF 0.3% topic match

0.3%

0.1

1998

[206] Development of the cerebral cortex: VI. growth factors: I. P. Lombroso Journal of the American Academy of Child and Adolescent Psychiatry 1998 - 3 citations - Show abstract - Cite Abstract: Earlier columns described how neurons are born and migrate to their final destination within the cerebral cortex. In the next stage of cortical development, axons and dendrites grow and form synapses. From birth to age 6 years, the child's brain grows dramatically (Fig. 1). This growth is not due to new neurons, as the vast majority of nerve cells are present at birth. Surprisingly, two thirds of all neurons born during fetal development will die during the first decade of life in a process termed apoptosis, or programmed cell death. The remarkable growth of the brain during these first few years is due primarily to the elongation ofaxons and an expansion in the number of dendrites as synapses are formed. The next several Development and Neurobiology columns will describe this process and how environmental factors may influence it. Exactly how a neuron forms its proper connections is an area of active research. The growing axonal tip interacts with its target neurons. Once a synapse has formed, the survival of both neurons depends on maintaining a close interaction. The development of synapses and the longterm survival of neurons are mediated by trophic factors that are secreted by the target nerve cells, bind to specific receptors, and signal to the nearby developing synapse. Within the nervous system, the most extensively studied of these factors is the family of neurotrophins. Almost 50 years ago, Rita Levi-Montalcini and Stanley Cohen isolated and identified nerve growth factor (NGF). This accomplishment earned them the Nobel Prize in Medicine in 1986. Four members of this family of neurotrophins are known to affect the growth and development of cells within the CNS. Scientists have discovered several simple rules that describe how neurotrophins influence the growth of neurons. First, neurons require trophic factors to survive. Neurons compete for the minute amounts of trophic factors that are produced. Experiments have shown that when NGF is added into tissue cultures or injected directly into the CNS, the number of neurons, as well as their axons and dendrites, increases dramatically. Antibodies that bind to and thereby inactivate NGF have the opposite effect and lead to neuronal death. 0.3% topic match

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82.4

1987

[207] The nerve growth factor 35 years later. R. Levi‐montalcini Science 1987 - 3067 citations - Show abstract - Cite Abstract: "Embryogenesis is in some way a model system. It has always been distinguished by the exactitude even punctitio, of its anatomical descriptions. An experiment by one of the great masters of embryology could be made the text of a discourse on scientific method. But something is wrong, or has been wrong. There is no theory of development in the sense in which Mendelism is a theory that accounts for the results of breeding experiments. There has therefore been little sense of progression or timeliness about embryological research. Of many papers delivered at embryological meetings, however good they may be in themselves . . . one too often feels that they might have been delivered five years beforehand without making anyone much the wiser, or deferred for five years without making anyone conscious of a great loss" (1). This feeling of frustration so incisively conveyed by these considerations by P. Medawar, pervaded, in the forties, the field of experimental embryology which had been enthusiastically acclaimed in the mid-thirties, when the upper lip of the amphibian blastopore brought this area of research to the forefront of the biological stage. The side branch of experimental neuroembryology, which had stemmed out from the common tree and was entirely devoted to the study of the tropic interrelations between neuronal cell populations and between these and the innervated organs and tissues, was then in its initial vigorous growth phase. It in turn suffered from a sharp decrease in the enthusiasm that had inflamed the pioneers in this field, ever since R. G. Harrison delivered his celebrated lecture on this topic at the Royal Society in London in 1935 (2). Although the alternate "wax and wane" cycles are the rule rather than the exception in all fields of human endeavor, in that of biological sciences the "wane" is all too often indicative of a justified loss of faith in the rational and methodical approach that had at first raised so much hope. A brief account of the state-of-the-art of experimental neuroembryology in the 0.3% topic match

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8.3

1997

[208] 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 - PDF 0.3% topic match

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3.2

1998

[209] Ex vivo nerve growth factor gene transfer to the basal forebrain in presymptomatic middle-aged rats prevents the development of cholinergic neuron atrophy and cognitive impairment during aging. Alberto Martínez-Serrano and A. Björklund Proceedings of the National Academy of Sciences of the United States of America 1998 - 85 citations - Show abstract - Cite 0.3% topic match

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14.4

1984

[210] Specific retrograde transport of nerve growth factor (NGF) from neocortex to nucleus basalis in the rat M. Seiler and M. Schwab Brain Research 1984 - 585 citations - Show abstract - Cite 0.3% topic match

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0.0

1996

[211] Enhancement of Neural Death by Nerve Growth Factor Jun‐mo Chung and Jinfang Hong Journal Not Provided 1996 - 0 citations - Show abstract - Cite 0.2% topic match

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17.6

2003

[212] Stimulation in Hippocampal Region CA1 in Behaving Rats Yields Long-Term Potentiation when Delivered to the Peak of Theta and Long-Term Depression when Delivered to the Trough James M. Hyman, ..., and M.E. Hasselmo The Journal of Neuroscience 2003 - 369 citations - Show abstract - Cite - PDF 0.2% topic match

0.2%

10.6

1996

[213] Neurotrophins and activity-dependent development of the neocortex T. Bonhoeffer Current Opinion in Neurobiology 1996 - 306 citations - Show abstract - Cite 0.2% topic match

0.1%

1.4

1991

[214] Exogenous Nerve Growth Factor Reverses Age‐Related Structural Changes in Neocortical Neurons in the Aging Rat R. Mervis, ..., and L. R. Williams Annals of the New York Academy of Sciences 1991 - 47 citations - Show abstract - Cite 0.1% topic match

0.1%

1.2

1998

[215] Competition for Neurotrophic Factors: Mathematical Analysis T. Elliott and N. Shadbolt Neural Computation 1998 - 30 citations - Show abstract - Cite 0.1% topic match

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1.1

2003

[216] 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 - PDF 0.1% topic match

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None

[217] Developmental and regional expression of f nerve growth factor messenger RNA and protein in the rat central nervous system S. Whittemore, ..., and H. Persson Journal Not Provided None - 132 citations - Show abstract - Cite Abstract: The presence of nerve growth factor (NGF) mRNA and protein in the rat central nervous system is documented. Blot-hybridization analysis showed an abundance of NGF mRNA in the hippocampus, cerebral cortex, and olfactory bulb. Enzyme immunoassay confirmed significant levels of a NGF-like protein in the hippocampus and cerebral cortex. Bioassay of a NGF-like immunoaffinity-purified protein from these regions was physiologically indistinguishable from NGF. Immunohistochemistry revealed a widespread distribution of NGF-like reactivity in the adult brain, preferentially in fiber tracts. NGF mRNA accumulation began at birth, with adult levels reached 3 weeks postnatally. Enzyme immunoassay detected the presence ofa NGF-like protein in the embryonic rat brain. Postnatally, the level of NGF-like protein reached a maximum at 3 weeks. Additionally, a distinct fetal form of NGF may exist. ,B nerve growth factor (NGF) is essential for the development and maintenance of sensory and sympathetic neurons in the peripheral nervous system (PNS) (1, 2). However, both the presence and potential physiological function of NGF in the central nervous system (CNS) has remained elusive (3). The characteristic responses of peripheral adrenergic neurons following NGF or anti-NGF antibody injection have not been observed after similar application into the CNS (4-11). In the PNS, NGF is taken up by adrenergic terminals and also retrogradely transported to the cell body (2). In the CNS, injected NGF was specifically retrogradely transported from the hippocampus to the medial septum and the diagonal band of Broca (9) and also from the neocortex to the nucleus basalis (12), presumably in cholinergic neurons. NGF induced choline acetyltransferase in neonatal rat cortex, hippocampus, septum (10), and striatum (11), but not in adult hippocampus (13). Thus, NGF may have a physiological function in the CNS, and affect cholinergic neurons. Initial indication of endogenous NGF in the CNS was obtained by immunohistochemistry in the fetal rat (14, 15). NGF cDNA clones have been isolated from male mouse submaxillary glands (16, 17), and Shelton and Reichardt (18) recently detected NGF mRNA in the rat brain. Subsequently, NGF mRNA and an NGF-like protein have been described in some regions of the adult rat brain (19). In the present study, we demonstrate the developmental time course as well as the adult regional distribution of both NGF mRNA and protein in the adult rat brain. Finally, using a bioassay, we show that the adult brain contains nerve growth-stimulating activity typical of purified NGF. Our results demonstrate that NGF is expressed in the adult rat CNS with regional specificity and suggests the existence of a fetal form of NGF. MATERIALS AND METHODS Preparation of RNA and Blot-Hybridization Analysis. Total RNA from the brains of Sprague-Dawley rats (Alab, Stockholm, Sweden) was prepared (20), and poly(A)+ RNA, isolated by oligo(dT) chromatography (21), was separated on 1% agarose gels containing 0.7% formaldehyde and transferred to nitrocellulose filters. The double-stranded DNA probe used to detect /3-NGF (hereafter referred to as NGF) was a 900-base-pair (bp) Pst I fragment derived from a NGF cDNA clone (16); the probe to detect c-myc was 1.3-kilobase (kb) Cla I-EcoRI fragment from the 3' exon of the human MYC gene (22); and the probe to detect a-actin was a 1.5-kb Pst I DNA fragment (23). Purified DNA fragments were nick-translated to a specific activity of 109 cpm/,ug, hybridized to the blotted nitrocellulose filters overnight, and washed at high stringency. Filters were exposed on Kodak XAR-5 x-ray film at -80°C. Known dilutions of poly(A)+ RNA from male mouse submaxillary glands were always included as standards. Autoradiograms were quantified by densitometry [Shimadzu (Kyoto, Japan) CS-390]. Immunoafflnity Chromatography ofRat Brain NGF. Cortex and hippocampus (100 g wet weight) from 100 adult female Sprague-Dawley rats were homogenized in 0.1 M Tris HCl, pH 8.0/0.5 M NaCl and centrifuged. The supernatant was applied to a 3-ml column of afflinity-purified anti-mouse NGF antibodies coupled to CNBr-activated Sepharose (Pharmacia). The column was washed extensively, and bound NGF was eluted with 0.1 M glycine HCl (pH 2.5) containing 0.02% bovine serum albumin, concentrated to 4 ml in the culture medium used for bioassay by pressure dialysis, sterilized by filtration, and tested for NGF activity. Quantitation of NGF in Rat Brain. Explanted ganglia bioassay. Chicken sympathetic ganglia (day 9 embryos) were explanted into a collagen matrix, and the rat brain immunoelutant was tested for NGF activity (24, 25). Cultures were examined with dark-field microscopy and scored for fiber outgrowth. Enzyme-linked immunoassayfor NGF. Immunoplates (96well black Microfluor plates, Dynatech, Alexandria, VA) were coated with affinity-purified antibodies against mouse NGF (25-27), and nonspecific binding was blocked with 1% bovine serum albumin. Brain samples in TBS buffer (0.02 M Tris HCl, pH 7.5/0.5 M NaCl) containing aprotinin, 0.1 mM phenylmethylsulfonyl fluoride, 0.1% bovine serum albumin, 10 mM EDTA, and 0.5% Tween 20 were added to the wells Abbreviations: NGF, nerve growth factor; PNS, peripheral nervous system; CNS, central nervous system; bp, base pair(s); kb, kilobase(s). §To whom reprint requests should be addressed. 817 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. 818 Neurobiology: Whittemore et al. 0.1% topic match

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0.3

2001

[218] Purification, crystallization and preliminary X-ray analysis of the Fab fragment from MNAC13, a novel antagonistic anti-tyrosine kinase A receptor monoclonal antibody. S. Covaceuszach, ..., and D. Lamba Acta crystallographica. Section D, Biological crystallography 2001 - 7 citations - Show abstract - Cite 0.0% topic match

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4.3

1989

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

0.0%

9.8

2003

[220] 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 - 207 citations - Show abstract - Cite - PDF 0.0% topic match

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