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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
Basic Fibroblast Growth Factor Evokes a Rapid Glutamate Release
through Activation of the MAPK Pathway in Cultured Cortical
Neurons*
Tadahiro
Numakawa §,
Daisaku
Yokomaku ,
Kazuyuki
Kiyosue¶,
Naoki
Adachi ,
Tomoya
Matsumoto ,
Yumiko
Numakawa ,
Takahisa
Taguchi¶,
Hiroshi
Hatanaka , and
Masashi
Yamada
From the 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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Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.
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