脑缺血损伤涉及多种病理过程,其中兴奋性毒性是关键机制之一。谷氨酸是脑内主要的兴奋性递质,谷氨酸及其受体的病理变化是引起兴奋性毒性的重要病理基础。该文综述了脑缺血后谷氨酸异常释放、谷氨酸受体表达变化及受体后信号传导等病理机制,及以上述机制为靶点的药物研究进展。
Many pathological process are involved in cerebral ischemia,and one of the key mechanisms is excitatory toxicity.As glutamate is an important excitatory neurotransmitter in brain,pathological changes of its receptors and itself are major basis of excitotoxicity.Abnormal release of glutamate after cerebral ischemia,altered expression of glutamate receptors and post-receptor signal transmission are reviewed,as well as research on drugs which target on the above mechanisms.