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Previous Article | Next Article
The Journal of Neuroscience, December 1, 2001, 21(23):9204-9213
Phosphorylation of cAMP Response Element-Binding Protein in Hippocampal Neurons as a Protective Response after Exposure to Glutamate In Vitro and Ischemia In Vivo
Takuma Mabuchi1, Kazuo Kitagawa1, Keisuke Kuwabara1, Kenichiro Takasawa1, Toshiho Ohtsuki1, Zhengui Xia3, 4, Daniel Storm4, Takehiko Yanagihara2, Masatsugu Hori1, and Masayasu Matsumoto1, 2 1 Division of Strokology, Department of Internal Medicine and Therapeutics and 2 Department of Clinical Neuroscience, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan, and Departments of 3 Environmental Health and 4 Pharmacology, University of Washington, Seattle, Washington 98195
Although accumulating evidence indicates that cAMP response element-binding protein (CREB) phosphorylation mediates not only synaptic plasticity but also survival of certain neurons, it remains uncertain whether CREB phosphorylation induced after metabolic insult leads to CRE-mediated gene transcription and is involved in cell survival or not. In the present study, we clarified that (1) CREB phosphorylation and ischemic tolerance induced after preconditioning ischemia in the hippocampal neurons was abolished by MK801 administration in gerbil global ischemia model, (2) CREB phosphorylation induced after exposure to glutamate in cultured neurons was inhibited by removal of extracellular calcium, by MK801 and by an inhibitor of calcium-calmodulin-dependent protein kinase (CaMK) II and IV, (3) inhibitor of CaMK II-IV or CRE-decoy oligonucleotide suppressed upregulation of BCL-2 expression and accelerated neuronal damage after exposure to glutamate, and (4) CREB phosphorylation induced in the hippocampal neurons after ischemia and in cultured neurons after exposure to glutamate was followed by CRE-mediated gene transcription in transgenic mice with a CRE-LacZ reporter. Our results suggest that CREB phosphorylation in neurons after ischemia and exposure to glutamate is induced by NMDA receptor-gated calcium influx and subsequent activation of CaMK II-IV and that CREB phosphorylation after metabolic stress might show a neuroprotective response through CRE-mediated gene induction.
Key words: CREB; ischemia; BCL-2;
-galactosidase; glutamate; CRE-decoy oligonucleotide
Copyright © 2001 Society for Neuroscience 0270-6474/01/21239204-10$05.00/0
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