摘要
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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2012年第6期747-750,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金重点项目(No 30830118)
"重大新药创制"科技重大专项(No 2009ZX09102-137
2012ZX09101-214)
关键词
脑缺血
兴奋性毒性
神经元
谷氨酸
谷氨酸受体
谷氨酸转运体
cerebral ischemia
excitotoxicity
neurons
glutamate
glutamate receptor
glutamate transporter