2002年6月
Neurotrophins induce BDNF expression through the glutamate receptor pathway in neocortical neurons
NEUROPHARMACOLOGY
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- 巻
- 42
- 号
- 7
- 開始ページ
- 903
- 終了ページ
- 912
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/S0028-3908(02)00043-6
- 出版者・発行元
- PERGAMON-ELSEVIER SCIENCE LTD
Neurotrophins jointly exert various functions in the nervous system, including neuronal differentiation. survival. and regulation of synaptic plasticity. However, the functional interactions of neurotrophins or mechanisms through which neurotrophins regulate each other are still not clear. In the present study, brain-derived neurotrophic factor (BDNF) mRNA expression is induced by neurotrophin-4/5 (NT-4/5) and by BDNF itself in neocortical neurons. K252a, a specific tyrosine kinase (Trk) inhibitor, completely suppresses BDNF- and NT-4/5-enhanced BDNF mRNA expression. NT-4/5 significantly augments BDNF protein production, which is also reversed by K252a. When neurons Lire incubated with neurotrophin-3 (NT-3) or nerve growth factor (NGF). there are no significant changes in BDNF mRNA or protein expression. Interestingly, the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor blocker 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or the N-methyl-D-aspartate (NMDA) receptor blocker AP-5 Completely Suppresses NT-4/5-enhanced BDNF protein production, while tetrodotoxin (TTX) only suppresses NT-4/5-enhanced BDNF production by 50%. Additionally, the mitogen activated protein (MAP) kinase inhibitor PD98059 enhances BDNF-induced glutamate receptor-1 (GluR1) protein expression. but a phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 strongly reduces BDNF-induced GluR1 protein expression. Taken together, glutamate receptors are important for the regulation of BDNF expression by neurotrophins. and MAP and PI3K kinases differentially modulate AMPA receptor expression in the cortical neurons. (C) 2002 Elsevier Science Ltd. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/S0028-3908(02)00043-6
- ISSN : 0028-3908
- PubMed ID : 12069900
- Web of Science ID : WOS:000177086600003