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Originally published In Press as doi:10.1074/jbc.M202927200 on May 28, 2002

J. Biol. Chem., Vol. 277, Issue 32, 28861-28869, August 9, 2002
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Basic Fibroblast Growth Factor Evokes a Rapid Glutamate Release through Activation of the MAPK Pathway in Cultured Cortical Neurons*

Tadahiro NumakawaDagger §, Daisaku YokomakuDagger , Kazuyuki Kiyosue, Naoki AdachiDagger , Tomoya MatsumotoDagger , Yumiko NumakawaDagger , Takahisa Taguchi, Hiroshi HatanakaDagger , and Masashi YamadaDagger

From the Dagger  Division of Protein Biosynthesis, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan, and the  Neuronics R. G. Division for Human Life Technology National Institute of Advanced Industrial Science and Technology (AIST) Midorigaoka, Ikeda, Osaka 563-8577, Japan

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.


§ Japan Society for the Promotion of Science Postdoctoral Fellow. To whom correspondence should be addressed: Division of Protein Biosynthesis, Inst. for Protein Research Osaka University, Suita, Osaka 565-0871, Japan. Tel.: 81-727-51-9524; Fax: 81-727-51-9628; E-mail: t-numakawa@aist.go.jp.


Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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