大鼠全脑缺血后海马CA1区锥体细胞DND的实验研究  

THE STUDY ON DND OF PYRAMIDAL CELLS IN HIPPOCAMPAL CA1 REGION FOLLOWINGGLOBAL ISCHEMIA IN RATS

作　　者：刘红梅[1] 佟振清[1] 张敬东[1] 高天明[1] 

机构地区：[1]第一军医大学生理学教研室

出　　处：《中国应用生理学杂志》1998年第3期201-204,共4页Chinese Journal of Applied Physiology

基　　金：国家自然科学基金;广东省自然科学基金

摘　　要：据报道，脑缺血损伤能导致迟发性神经元死亡（ｄｅｌａｙｅｄｎｅｕｒｏｎａｌｄｅａｔｈ，ＤＮＤ）。有学者认为ＤＮＤ是神经兴奋毒性作用引起的细胞坏死过程，也有学者认为主要是凋亡机制参与了ＤＮＤ。我们研究发现，大鼠全脑缺血１５ｍｉｎ后再灌流４８ｈ，海马ＣＡ１区锥体细胞大量死亡，其超微结构出现细胞膜完整的胞浆浓缩和核固缩的凋亡样形态学改变，并且蛋白合成抑制剂放线菌酮对ＣＡ１区锥体细胞的脑缺血损伤具有明显的保护作用。说明脑缺血后锥体细胞的死亡需要一定的时间合成新的蛋白质，从而激活细胞内部死亡程序。提示凋亡机制参与全脑缺血后ＤＮＤ。AbstractAbstract:It was reported that ischemia induced delayed neuronal death(DND).Some authors consider DND as necrosis mediated by excitotoxicity,others consider apoptosis contributes importantly to DND.Our present work demonstrates a lot of pyramidal cells of CA1 region in hippocampus will die 48 h after reperfusion following 15 min global ischemia in rats.The ultrastructure of these pyramidal cells shows apoptosislike changes with condensed cytoplasm, pyknotic nucleus and intact cytomembrane. Furthermore the protein synthesis inhibitorcycloheximide could prevent CA1 pyramidal cells from DND remarkably,which implies a certain time will be required after ischemia for pyramidal cells to synthesize new proteins to activate the cellular death program.It suggests that apoptosis may be involved in DND following global ischemia. KEY WORDS ischemia; DND; hippocampus; apoptosis; ultrastructure; cycloheximide

关 键 词：脑缺血 海马 细胞凋亡 超微结构 放线菌酮 

分 类 号：R743.3[医药卫生—神经病学与精神病学]