PMID:12034732

Citation	Numakawa, T, Yokomaku, D, Kiyosue, K, Adachi, N, Matsumoto, T, Numakawa, Y, Taguchi, T, Hatanaka, H and Yamada, M (2002) Basic fibroblast growth factor evokes a rapid glutamate release through activation of the MAPK pathway in cultured cortical neurons. J. Biol. Chem. 277:28861-9
Abstract	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 Ca2+ concentration through voltage-dependent Ca2+ 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.
Links	PubMed Online version:10.1074/jbc.M202927200
Keywords	Amino Acids/metabolism; Animals; Calcium/metabolism; Cell Division; Dose-Response Relationship, Drug; Enzyme Activation; Exocytosis; Fibroblast Growth Factor 2/metabolism; Fibroblast Growth Factors/metabolism; Glutamic Acid/metabolism; Immunoblotting; Immunohistochemistry; MAP Kinase Signaling System; Microscopy, Fluorescence; Neurons/metabolism; Potassium/metabolism; Rats; Signal Transduction; Sodium/metabolism; Tetanus Toxin/metabolism; Time Factors
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