胶质细胞谷氨酸转运体及其在脑缺血和脑缺血预适应中的变化  

Glial glutamate transporters and its change in brain ischemia and cerebral ischemic preconditioning

作　　者：张敏[1] 李文斌[1] 王彦华[2] 

机构地区：[1]河北医科大学病理生理学教研室,石家庄050017 [2]河北工程大学医学院,邯郸056002

出　　处：《生命科学》2010年第5期431-436,共6页Chinese Bulletin of Life Sciences

基　　金：国家自然科学基金项目(30770738);河北省自然科学基金项目(C2008001042;C2010000478);河北省应用基础研究设计重点基础研究项目(09966109D);河北省教育厅自然科学项目(2009143);河北医科大学科研骨干人才计划(30900092)

摘　　要：兴奋性氨基酸转运体(excitatory amino acid transporters,EAATs)是摄取细胞外液谷氨酸、保持细胞外谷氨酸低浓度的主要机制,已发现了五种EAATs,其中胶质细胞谷氨酸转运体在终止谷氨酸能神经传递、维持细胞外液谷氨酸浓度处于低水平方面发挥更重要作用。胶质细胞谷氨酸转运体的表达和功能受谷氨酸及其受体、垂体腺苷酸环化酶激活多肽、生长因子、内皮素、一氧化氮等许多因素的影响,其表达减少及功能降低与脑缺血损害的发生和发展密切相关,脑缺血预适应可通过调控其表达或改善其功能而诱导脑缺血耐受。Excitatory amino acid transporters （EAATs） are the primary mechanism for clearance of glutamate in the extracellular fluid. Five kinds of EAATs have been found. Although both neurons and glia contain EAATs, it is generally accepted that the uptake capacity of astrocytes is much higher than that of neurons. Both the expression and the function of glial glutamate transporters are regulated by many factors such as glutamate and its receptors, pituitary adenylate cyclase-activating polypeptide, growth factors, endothelins, nitric oxide, etc. The decreased expression and dysfunction of glial glutamate transporters are tightly correlated with neuronal damages induced by brain ischemia. Through regulating the expression and improving the function of EAATs, cerebral ischemic preconditioning can induce brain ischemic tolerance.

关 键 词：谷氨酸 兴奋性氨基酸转运体 脑缺血 脑缺血预适应 

分 类 号：R363[医药卫生—病理学] R338.2[医药卫生—基础医学]