血管性痴呆模型大鼠海马CA3区微管相关蛋白-2的表达及其意义

The Map-2 Expression Levels in Hippocampal Ca3 Region in Rat Model of Vascular Dementia

目的:探讨海马CA3区神经元微管相关蛋白-2(MAP-2)表达变化与学习记忆功能的关系。方法:采用大白鼠大脑中动脉线栓法(MCAO)缺血再灌模型,分为缺血2h再灌(I/R)1d、7d、14d、30d、90d组和假手术组,免疫组织化学方法观察海马CA3区MAP-2表达,并用图像分析系统作定量分析;同时用Morris水迷宫检测再灌7d、14d、30d、90d组大鼠行为学变化。结果:缺血再灌1d海马CA3区MAP-2呈高表达突起断裂不均匀,再灌7d和14d表达最高,突起出现螺旋样变,再灌30d后MAP-2的表达开始恢复,突起依然断裂,再灌90d后突起形态基本恢复正常。行为学检测发现,大白鼠缺血再灌7d和14d组定位航行试验潜伏期明显延长,空间探索试验中跨平台次数减少,再灌30d开始恢复,再灌90d与假手术组无差别。结论:缺血再灌后,海马CA3区神经元处于高度可塑性状态,可能是神经元新的突触连接形成的结构基础之一,可部分代偿缺血敏感区CA1神经元丧失引起的学习记忆功能的下降。

Objective： To investigate the MAP-2 expression levels in CA3 region ofhippocampus, and its relation to spatial learning and memory function in rat model of vascular dementia. Methods： Unilateral cerebral ischemia was induced by permanent occlusion of the distalmiddle cerebralartery. Sixty Wistar rats were divided randomly into ischemia-reperfusion group （I/R） and sham group. Ac- cording to the animal surviving period, observations were made in 1, 7d, 14d, 30 and 90d after ischemia 2h. These rats were tested by Morris water maze before sacrified. The expression of MAP-2 in hippocampal CA3 region was detected by immunohistochemistry and the intensity of immunostaining was measured using MedHPIAS pathologic imaging-analysis system. Results： The result indicated the high expression of MAP-2 in I/R ld group （P〈0.01） with dendrite fragmentation. The expressions of MAP-2 in I/R 7d and 14d group were highest （P〈0.01） with dendrite screwing. There was no difference between I/R 30d and sham group （P〉0.05）, but dendrite fragmenration could also be observed in I/R 30d group. The shape of the dendrite was back to normal in I/R 90d group. The observation of behav- ior in Morris water maze indicated that the latency of localization navigation were longer obviously and the cross platform number of times reduced in I/R 7d and 14d group （P〈0.01）. The latency restored in I/R 30d group, and have also no difference compared to sham group in I/R 90d group （P〉0.05）. Conclusions： The results showed that the neuronal plasticity in hippocampal CA3 areas after ischemi- a-reperfusion may be a structure foundation of the new synapse formation, and could partially repair learning and memory function.