慢性脑低灌注大鼠认知功能和突触可塑性变化

Cognitive impairment and changes of neuronal plasticity in rats of chronic cerebral hypoperfusion

目的建立一种与脑动静脉畸形有关的慢性脑低灌注动物模型,研究慢性脑低灌注对大鼠认知功能和突触可塑性变化的影响。方法建立慢性脑低灌注动物模型并设立鼠龄相匹配的对照组,术后3个月,采用水迷宫实验评价各组动物认知功能,神经可塑性采用免疫组化和蛋白印迹方法检测各组动物海马区组织中MAP-2,GAP-43和突触素表达。结果水迷宫实验检测发现模型组动物寻找平台的潜伏期较对照组明显延长,模型组动物在平台象限停留时间和跨越平台象限次数较对照组明显减少。模型组动物海马组织中MAP-2和突触素的表达较对照组明显降低,而两组动物之间GAP-43的表达水平未见明显差异。结论慢性脑低灌注可诱导大鼠认知功能障碍,可能与动物海马组织中MAP-2和突触素表达减少有关。

Objective A new cerebral arteriovenous malformations ( AVMs) rat model was developed to study the effect of chronic cerebral hypoperfusion on cognitive function and neuronal plasticity in rats. Methods Agedmatched animals comprised a control group. Three months after surgery,Morris water waze test was performed to evaluate the cognitive function in rats. Neuronal plasticity was assessed by measuring the protein expression of MAP-2, GAP-43 and synaptophysin in the hippocampal regions of rats with immunohistochemistry and western blotting. Results The average time of escape latency was significantly longer in the model rats than that in the control rats,and both the time spent in the platform quadrant and the frequency of original platform crossing during space probe trials were less than those in the control animals. The expression levels of MAP-2 and synaptophysin protein in hippocampal areas in the model rats were less than those in the control rats. However,there was no difference on the GAP-43 expression between the two groups. Conclusion These data suggested that chronic cerebral hypoperfusion associated with AVMs could lead to cognitive impairment in rats,which may be partially explained by reduced expression of MAP-2 and synaptophysin at the protein level in the hippocampal area.