期刊
BRAIN RESEARCH
卷 1020, 期 1-2, 页码 196-203出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2004.06.035
关键词
NMDA receptor; NR2B; glycogen synthase kinase-3; calcium ion; ifenprodil; apoptosis
The N-methyl-D-aspartate (NMDA) receptor 2B-selective antagonist ifenprodil induced morphological changes which were characterized by cell shrinkage, nuclear condensation or fragmentation, and internucleosomal DNA fragmentation in rat cultured cortical cells. Ifenprodil increased the apoptotic, cell death in a dose-dependent manner (0.5-10 muM). In addition, the protein synthesis inhibitor cycloheximide completely blocked ifenprodil-induced apoptotic cell death. The selective inhibitors of glycogen synthase kinase-3 (GSK-3) prevented the ifenprodil-induced apoptosis. Moreover, activation of caspase-3 was accompanied by cell death induced by ifenprodil in a dose-dependent manner. The ifenprodil-induced apoptosis was prevented by a caspase-3 inhibitor. These results suggested that activation of GSK-3 involves in the apoptosis induced by blocking of trophic effect of NMDA receptor consisting of NR2B subunit in rat cortical neurons. (C) 2004 Elsevier B.V. All rights reserved.
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