期刊
NEUROSCIENTIST
卷 11, 期 1, 页码 37-49出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1073858404269012
关键词
NMDA; excitotoxicity; NR2A; NR2B; Huntington's disease; Parkinson's disease; epilepsy; MAPK; Calpain; Calmodulin
资金
- NIMH NIH HHS [T32 MH 14654] Funding Source: Medline
- NINDS NIH HHS [NS45986] Funding Source: Medline
N-methyl-D-aspartate (NMDA) receptors are the major mediator of excitotoxicity. Although physiological activation of the NMDA receptor is necessary for cell survival, overactivation is a signal for cell death. Several pathways are activated through NMDA receptor stimulation. most of which can contribute to excitotoxicity. These include events leading to mitochondrial dysfunction, activation of calcium-dependent enzymes, and activation of mitogen-activated protein kinase pathways. Understanding the role of these mechanisms is important in developing agents that block excitotoxicity without inhibiting functions necessary for survival. NMDA receptor subtypes may be responsible for mediating separate pathways, and subtype-specific inhibition has shown promising results in some neurological models. This review examines the roles of NMDA receptor subtypes in excitotoxicity and neurological disorders.
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