N-甲基-D-天冬氨酸受体在脑中风发病机制中的作用研究进展

Function of N-Methyl-D-Aspartic Acid Receptors in Cerebral Stroke

综合近年的文献,陈述并总结近年来N-甲基-D-天冬氨酸(N-methyl-D-aspartic acid,NMDA)受体在脑中风发病机制中的作用,以NMDA受体为靶点,介绍其结构、在缺血性脑中风损伤及神经再生中的作用,以及相关干预剂的抗中风研究进展。为药物开发提供理论基础。NMDA受体在中风病理过程中表现出双重性,其过度激活参与了兴奋性毒性的产生,损害机体;而另一方面,其又参与了缺血后神经再生的活动,有利于机体修复。寻找调控NMDA受体的信号因子及揭示NMDA受体所调控的下游信号,使双重性中的损伤因素被抑制而保护/修复机制被激活的相关机制;开发相应药物是今后研究工作的重点。

Cerebral stroke is caused by the interrupt of blood supply either by the blockage or by the rupture of the brain blood ves- sels. After the activation of the ischemic cascades, a series of neurochemical reactions might occur which involves the excess release of the excitatory amino acids. The ionotropie glutamate receptor of N-methyl-D-aspartic acid subtype （ NMDA receptor） has been proven to play dual roles in the ischemic insults. On one hand, NMDA receptor has been proven to initiate the ischemie impairment, leading to the neuronal death. On the other hand, NMDA receptor is involved in the endo-neurogenesis process after the ischemic onset. Here- in. we summarized the recent studies about the structures and functions of NMDA receptor in ischemie stroke pathogenesis.