脑缺血时谷氨酸释放机制  

The mechanisms of glutamate release in cerebral ischemia

作　　者：梅和珊[1] 王永利[1] 

机构地区：[1]河北医科大学药理学教研室,河北石家庄050017

出　　处：《中国药理学通报》2005年第4期393-396,共4页Chinese Pharmacological Bulletin

摘　　要：谷氨酸是中枢神经系统主要的兴奋性神经递质,在脑缺血造成的神经元损伤过程中发挥重要作用。脑缺血时多种机制参与了谷氨酸释放的的调节,如Ca2+依赖性的出胞式释放、谷氨酸转运体调节的释放、水肿诱发的释放和受体调节的释放等。本文根据现有的文献资料,综述了脑缺血时谷氨酸释放机制。Glutamate is a major excitatory neurotransmitter in the central nervous system(CNS)and plays an important role in neuronal damage induced by cerebral ischemia. Several mechanisms contribute to modulation of glutamate release during cerebral ischemia, such as vesicular release dependent on calcium, release by reversed operation of glutamate transporters, release through swelling-activated anion channel and receptor-modulating release, etc. This review addresses the mechanisms of glutamate release during cerebral ischemia.

关 键 词：脑缺血 谷氨酸 Γ-氨基丁酸受体 谷氨酸转运体 代 谢型谷氨酸受体 胱氨酸-谷氨酸转运体 

分 类 号：R-05[医药卫生] R329.25