Fibroblast Growth Factor Enhances Long‐term Potentiation in the Hippocampal Slice

Terlau, Heinrich; Seifert, W.

doi:10.1111/j.1460-9568.1990.tb00009.x

Cited by 81 publications

(27 citation statements)

References 28 publications

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“…Based on these observations, we propose that NgR1 functions as a liganddependent regulator of long-lasting activity-induced changes in synaptic strength. Although previous studies have reported FGF2-elicited enhancement of LTP in CA1 neurons after tetanic stimulation in rat (Terlau and Seifert, 1990), we did not observe FGF2-dependent changes in HFS-induced LTP in wild-type mice. So, does FGF2 function at the synapse?…”

Section: Ngr1 Regulates Activity-dependent Synaptic Strengthcontrasting

confidence: 52%

“…The previously reported role of FGF2 in modulating synaptic function in the hippocampus (Terlau and Seifert, 1990) coupled with the colocalization of NgR1, FGFR1, and FRS2␣ at postsynaptic sites prompted us to investigate whether physiological NgR1 signaling modulates synaptic transmission in the presence of exogenously applied FGF2.…”

Section: Ngr1 Regulates Hippocampal Ltp In An Fgf2-dependent Mannermentioning

confidence: 99%

“…Fibroblast growth factors (FGFs) comprise a large family of polypeptides, members of which regulate a plethora of cellular processes during neural development and adulthood (Mason, 2007). The prototypic family member, FGF2, promotes axonal growth and sprouting after injury (Fagan et al, 1997) and has also been found to influence hippocampal synaptic plasticity (Terlau and Seifert, 1990).…”

Section: Introductionmentioning

confidence: 99%

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Synaptic Function for the Nogo-66 Receptor NgR1: Regulation of Dendritic Spine Morphology and Activity-Dependent Synaptic Strength

Lee¹,

Raiker²,

Venkatesh³

et al. 2008

J. Neurosci.

152

210

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In the mature nervous system, changes in synaptic strength correlate with changes in neuronal structure. Members of the Nogo-66 receptor family have been implicated in regulating neuronal morphology. Nogo-66 receptor 1 (NgR1) supports binding of the myelin inhibitors Nogo-A, MAG (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), and is important for growth cone collapse in response to acutely presented inhibitors in vitro. After injury to the corticospinal tract, NgR1 limits axon collateral sprouting but is not important for blocking long-distance regenerative growth in vivo. Here, we report on a novel interaction between NgR1 and select members of the fibroblast growth factor (FGF) family. FGF1 and FGF2 bind directly and with high affinity to NgR1 but not to NgR2 or NgR3. In primary cortical neurons, ectopic NgR1 inhibits FGF2-elicited axonal branching. Loss of NgR1 results in altered spine morphologies along apical dendrites of hippocampal CA1 neurons in vivo. Analysis of synaptosomal fractions revealed that NgR1 is enriched synaptically in the hippocampus. Physiological studies at Schaffer collateral-CA1 synapses uncovered a synaptic function for NgR1. Loss of NgR1 leads to FGF2-dependent enhancement of long-term potentiation (LTP) without altering basal synaptic transmission or short-term plasticity. NgR1 and FGF receptor 1 (FGFR1) are colocalized to synapses, and mechanistic studies revealed that FGFR kinase activity is necessary for FGF2-elicited enhancement of hippocampal LTP in NgR1 mutants. In addition, loss of NgR1 attenuates long-term depression of synaptic transmission at Schaffer collateral-CA1 synapses. Together, our findings establish that physiological NgR1 signaling regulates activity-dependent synaptic strength and uncover neuronal NgR1 as a regulator of synaptic plasticity.

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Section: Ngr1 Regulates Activity-dependent Synaptic Strengthcontrasting

confidence: 52%

Section: Ngr1 Regulates Hippocampal Ltp In An Fgf2-dependent Mannermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Synaptic Function for the Nogo-66 Receptor NgR1: Regulation of Dendritic Spine Morphology and Activity-Dependent Synaptic Strength

Lee¹,

Raiker²,

Venkatesh³

et al. 2008

J. Neurosci.

152

210

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“…Indeed, bFGF modulates the efficacy of hippocampal synaptic transmission. bFGF enhances the generation of long term potentiation in hippocampal neurons (15,16). These findings suggest that bFGF is involved in glutamatergic transmission, because it is widely accepted that the release of glutamate (presynaptic), as well as the NMDA and the AMPA receptor (postsynaptic), is essential for long term potentiation (17,18).…”

mentioning

confidence: 86%

Basic Fibroblast Growth Factor Evokes a Rapid Glutamate Release through Activation of the MAPK Pathway in Cultured Cortical Neurons*

Numakawa¹,

Yokomaku²,

Kiyosue³

et al. 2002

Journal of Biological Chemistry

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We examined the possibility that basic fibroblast growth factor (bFGF) is involved in synaptic transmissions. We found that bFGF rapidly induced the release of glutamate and an increase in the intracellular Ca 2؉ concentration through voltage-dependent Ca 2؉ channels in cultured cerebral cortical neurons. bFGF also evoked a significant influx of Na ؉ . Tetanustoxin inhibited the bFGF-induced glutamate release, revealing that bFGF triggered exocytosis. The mitogen-activated protein kinase (MAPK) pathway was required for these acute effects of bFGF. We also found that pretreatment with bFGF significantly enhanced high K ؉ -elicited glutamate release also in a MAPK activation-dependent manner. Therefore, we propose that bFGF exerts promoting effects on excitatory neuronal transmission via activation of the MAPK pathway.Neuronal transmissions require mechanisms that modulate the balanced interaction of multiple factors, which control functional maintenance and plasticity in the central nervous system. Many factors including growth factors and the excitatory amino acid glutamate control neuronal functions. In particular, brain-derived neurotrophic factor (BDNF, 1 one of the neurotrophins) plays a fundamental role in neuronal transmission and plasticity (1-7). We also reported that rapid glutamate release was induced by BDNF through the glutamate transporter in cultured cerebellar and cortical neurons (8, 9). However, very little work has been done concerning the roles of other neurotrophic factors in the acute modulation of central nervous system and peripheral nervous system functions (10, 11). Initially, bFGF was identified as an angiogenic mitogen, but it is now recognized as a neurotrophic factor. For example, it has been found that bFGF exerts neurotrophic activities in cortical and hippocampal neurons (12, 13). However, the expression of bFGF in the central nervous system increases during postnatal development (14), implying that bFGF also has important roles in synaptic maturation. Indeed, bFGF modulates the efficacy of hippocampal synaptic transmission. bFGF enhances the generation of long term potentiation in hippocampal neurons (15, 16). These findings suggest that bFGF is involved in glutamatergic transmission, because it is widely accepted that the release of glutamate (presynaptic), as well as the NMDA and the AMPA receptor (postsynaptic), is essential for long term potentiation (17,18). Several reports have indicated that these ionotropic glutamate receptor activities were regulated by bFGF. bFGF regulates the intracellular Ca 2ϩ concentration after activation of the NMDA receptor (19). Long term treatment with bFGF decreases the NMDA receptor-dependent increase in the Ca 2ϩ concentration, and the Ca 2ϩ attenuation is required for the neuroprotective effects in excitotoxic cell death (20, 21). The expression of the glutamate receptor protein is also changed by bFGF. bFGF increased the AMPA receptor subunit GluR1 protein but did not alter levels of GluR2/3, GluR4, or the NMDA subunit NR1 (22). The expres...

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“…Neurotrophic factors are proteins that stimulate neuronal growth and differentiation in the developing brain and that are now known to play a critical role in the survival, maintenance, and morphological plasticity of adult neurons (see Hefti et al 1993). Neurotrophic factors have been implicated in different forms of experience-dependent plasticity, including long-term potentiation (Terlau and Seifert 1990;Ishiyama et al 1991;Korte et al 1998;Chen et al 1999), learning (Zhang et al 1997a;Kesslak et al 1998;Mu et al 1999) and recovery of function (Chadi et al 1993;Rowntree and Kolb 1997).…”

Section: Neurotrophic Factors and The Effects Of Stimulant Drugsmentioning

confidence: 97%

Basic fibroblast growth factor as a mediator of the effects of glutamate in the development of long-lasting sensitization to stimulant drugs: studies in the rat

Flores¹,

Stewart²

2000

Psychopharmacology

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We argue that repeated exposure to stimulant drugs increases the demands on dopaminergic cell functioning, and, by stimulating glutamate release, recruits neurotrophic and neuroprotective substances such as bFGF. We propose that the actions of these factors, in turn, give rise to long-lasting neuronal adaptations that underlie sensitized responding to further drug exposure. Possible mechanisms whereby bFGF participates in the development of sensitization, including interactions with other neurotrophic factors, are discussed. In addition, we show how the evidence reviewed in this paper provides further support for the idea that repeated treatment with stimulant drugs induces synaptic plasticity.

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Fibroblast Growth Factor Enhances Long‐term Potentiation in the Hippocampal Slice

Cited by 81 publications

References 28 publications

Synaptic Function for the Nogo-66 Receptor NgR1: Regulation of Dendritic Spine Morphology and Activity-Dependent Synaptic Strength

Synaptic Function for the Nogo-66 Receptor NgR1: Regulation of Dendritic Spine Morphology and Activity-Dependent Synaptic Strength

Basic Fibroblast Growth Factor Evokes a Rapid Glutamate Release through Activation of the MAPK Pathway in Cultured Cortical Neurons*

Basic fibroblast growth factor as a mediator of the effects of glutamate in the development of long-lasting sensitization to stimulant drugs: studies in the rat

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