慢性前脑缺血致血管性痴呆大鼠神经元超微结构的经时变化  

Ultrastructure of the cerebral cortex and hippocampus of vascular dementia rats following chronic forebrain ischemia at different stage

作　　者：张海宁[1] 吴江[1] 孙莉[1] 王明宇[1] 汤跃宇[1] 

机构地区：[1]吉林大学第一医院神经内科,吉林长春130021

出　　处：《中风与神经疾病杂志》2009年第1期37-40,共4页Journal of Apoplexy and Nervous Diseases

基　　金：国家自然科学基金资助项目(No.30770756)

摘　　要：目的观察慢性前脑缺血致血管性痴呆大鼠额叶皮层、海马神经元不同时间点的超微结构改变。方法采用双侧颈总动脉永久结扎方法(2VO)制备慢性前脑缺血动物模型,于术后不同时间点(1月、2月、3月、4月)电镜观察额叶皮层、海马区结构改变。结果额叶皮层:1月时见额叶皮层大量脂褐素,2月有所下降,后与假手术对照组相仿,暗神经元则在2月时最多,后下降;海马区神经元胞质溶酶体逐渐增多,术后3月时暗神经元大量增多,并且出现大量脂褐素,术后4月神经元出现固缩。结论电镜下脂褐素和暗神经元的改变提示慢性脑缺血初期脑损伤是可逆的,电镜下1个月或更早可能是可逆损伤的转折点。Objective To observe the ultrastrncture of the cerebral cortex and hippocampus of vascular dementia （VD） rats following chronic forebrain isehemia at different stages. Methods We utilized the rat model of VD caused by permanent occlusion of bilateral common carotid arteries （2VO） , and observed the ultrastructure by transmission electron microscopy at different stages（ 1 m ,2m,3m ,4m） after the operation. Results In frontal cortex we found that there was a lot of lipofuscin in 1 m, and the number declined in 2m;then it was similar to the sham-treated control group. While the number of dark neurons reach the top in 2m and then decreased. In hippocampus we observed that lysosome in the cytoplasm of neurons increased as time;dark neurons teemed and lipofuscin presented in large numbers in 3m; nuclei became pyknotie in 4m. Conclusion The changes of lipofuscin and lysosome viewed by electron microscopy suggested that brain damage in initial stage of the chronic forebrain ischemia was reversible, and 1 month or earlier after operation may be the turning point.

关 键 词：脑缺血 慢性 超微结构 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]