Are Nerve Growth Factors Involved in Long-Term Synaptic Potentiation in the Hippocampus and Spatial Memory?

Sastry, B.R.; Chirwa, S.S.; May, P. B. Y.; Maretić, H.; Pillai, Gopal S; Kao, E. Y. H.; Sidhu, S. D.

doi:10.1007/978-3-642-73202-7_30

Cited by 9 publications

(3 citation statements)

References 16 publications

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“…Previous data suggested that growth factors may play roles in processes such as learning and memory. For example, Sastry and coworkers have shown that NGF and other unidentified proteins can modify LTP in the hippocampus (Sastry et al, 1988;Xie et al, 1991). The present data provide evidence that bFGF can influence a transmitter receptor believed to play a central role in the postsynaptic calcium influx involved in LTP (Malenka et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Basic FGF regulates the expression of a functional 71 kDa NMDA receptor protein that mediates calcium influx and neurotoxicity in hippocampal neurons

Mattson¹,

Kumar²,

Wang³

et al. 1993

J. Neurosci.

194

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Basic fibroblast growth factor (bFGF) was recently found to modulate the outgrowth-regulating effects of glutamate, and protected neurons from several brain regions against excitotoxi/ischemic damage. We provide evidence that the excitoprotective mechanism of bFGF involves suppression of the expression of a 71 kDa NMDA receptor protein (NMDARP- 71). NMDARP-71 protein and mRNA levels were reduced in neurons in bFGF- treated hippocampal cell cultures. The levels of the NMDARP-71 were not reduced by NGF or epidermal growth factor, and bFGF did not reduce the level of mRNA for the GluR1 kainate/AMPA receptor, demonstrating the specificity of the effect of bFGF on the NMDARP-71. The reduction in NMDARP-71 expression in bFGF-treated neurons was correlated with reduced vulnerability to NMDA neurotoxicity. A major role for NMDARP-71 in calcium responses to NMDA and excitotoxicity was demonstrated using antisense oligonucleotides directed against NMDARP-71. Northern and Western blot analysis and immunocytochemistry showed that NMDARP-71 antisense oligonucleotides caused a selective suppression of NMDARP-71 mRNA and protein levels during 12–44 hr exposure periods. Elevations in intracellular calcium levels normally caused by glutamate and NMDA were attenuated in neurons exposed to NMDARP-71 antisense oligonucleotide; calcium responses to kainate were relatively unaffected. NMDARP-71 antisense oligonucleotides protected the neurons against excitotoxicity. Thus, NMDARP-71 is a necessary component of an NMDA receptor mediating calcium responses and neurotoxicity in hippocampal neurons. Taken together, these data identify a mechanism whereby bFGF can modify neuronal responses to glutamate, and suggest that regulating the expression of excitatory amino acid receptors may provide a means for growth factors to influence the plasticity and degeneration of neural circuits.

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Section: Discussionmentioning

confidence: 99%

Basic FGF regulates the expression of a functional 71 kDa NMDA receptor protein that mediates calcium influx and neurotoxicity in hippocampal neurons

Mattson¹,

Kumar²,

Wang³

et al. 1993

J. Neurosci.

194

View full text Add to dashboard Cite

show abstract

“…Injury also increases the production of neurotrophic factors in the hippocampus (Collins and Crutcher, 1985). In addition, growth factors may modify neural activity since bFGF, IGFs, and NGF can attenuate glutamate-induced elevations of [Ca2+l, (Mattson et al, 1989;Mattson, 1991, 1992a), and FGF (Terlau and Seifert, 1989a), epidermal growth factor (EGF) (Terlau and Seifert, 1989b), and NGF (Sastry et al, 1988) can alter long-term potentiation, suggesting that these growth factors modulate glutamatergic signaling in the developing and adult hippocampal system.…”

Section: Growth Factorsmentioning

confidence: 99%

“…In addition, studies within the last 10 years have provided convincing evidence that neurotransmitters, previously thought to play roles only at the mature synapse, can influence neurite outgrowth and the structural organization of synaptic connections (Mattson, 1988;Meier et al, 1991). Similarly, growth factors previously thought to influence only cell survival and neurite outgrowth may also play roles in information coding at synapses (Sastry et al, 1988;Terlau and Seifert, 1989). Recent studies have shown that the regulation of free intracellular calcium levels ([Ca2'],) plays a pivotal role in controlling the neuronal growth cone (Kater et al, 1988) and in synaptic plasticity (Kennedy, 1989) and that misregulation of [Ca2+ 1, is involved Correspondence and reprint requests to Dr. Mark P. Mattson,211 Sanders-Brown Building, University of Kentucky, Lexington, KY 40536-0230 U .S .A.…”

mentioning

confidence: 99%