非谷氨酸受体依赖的钙毒性机制在急性脑缺血损伤中的作用  

Glutamate receptor-independent calcium toxicity pathways in acute ischemic brain injury

作　　者：向军[1] 唐宇平[1] 蔡定芳[1] 

机构地区：[1]复旦大学附属中山医院中西医结合科,复旦大学中西医结合研究所神经病学研究室,上海200032

出　　处：《中国病理生理杂志》2010年第6期1224-1228,共5页Chinese Journal of Pathophysiology

基　　金：上海市卫生系统百人计划项目;上海市医学领军人才资助项目(No.97BR016)

摘　　要：Intracellular Ca2+ overload and the following Ca2+-toxicity are an important mechanism underlying ischemic brain injury.However,recent clinical trials using antagonists of the N-methyl-daspartate(NMDA) to prevent ischemic brain injury in humans have been largely disappointing.Activation of glutamate receptors resulting in intracellular Ca2+ overload and excitotoxicity couldn’t explain the whole process of ischemic brain injury,and emerging new studies have suggested that activation of several glutamate receptor-independent Ca2+-toxicity pathways also contribute to ischemic brain injury.This review focus on the roles of acid sensing ion channels(ASICs),Na+-Ca2+ exchanger(NCX) and transient receptor potential(TRP) channels in the ischemic brain injury.Intracellular Ca2＋ overload and the following Ca2＋ - toxicity are an important mechanism underlying ischemie brain injury. However, recent clinical trials using antagonists of the N -methyl -daspartate （NMDA） to prevent ischemie brain injury in humans have been largely disappointing. Activation of glutamate receptors resulting in intraeellular Ca2 ＋ overload and exeitotoxicity couldn＇t explain the whole process of ischemic brain injury, and emerging new studies have suggested that activation of several glutamate receptor - independent Ca2＋ - toxicity pathways also contribute to isehemie brain injury. This review focus on the roles of acid sensing ion channels （ASICs） , Na＋- Ca2 ＋ exchanger （NCX） and transient receptor potential （TRP） channels in the isehemie brain injury.

关 键 词：酸敏感离子通道 Na+-Ca2+交换体 瞬时受体电位 脑缺血 钙 

分 类 号：R743[医药卫生—神经病学与精神病学]