摘要
目的建立血管性痴呆 (VD)的动物模型,并探讨血管性痴呆认知障碍的发病机制。方法采用持久性双侧颈总动脉结扎法致老龄大鼠慢性前脑血流灌注不足 ,建立老龄大鼠血管性痴呆模型 ,进行数字减影血管造影(DSA)检查、穿梭箱试验和胆碱乙酰转移酶 (Cholineacetyltransferase,ChAT)免疫组化测定。结果慢性脑血流灌注不足2月后出现明显的认知功能障碍 ,缺血4月后更明显 ;海马CA1区ChAT免疫反应阳性神经元分布及其数量较对照组显著减少 ,且与学习记忆障碍呈正相关。结论此模型能可靠模拟人的慢性脑血流灌注不足之血管性痴呆 ,其额叶皮层和海马胆碱能神经元的损伤可能是认知功能受损害的形态学基础。
Objective To establish an animal model of vascular dementia(VD) in aging rat and study the mechanism of hypomnesis in vascular dementia. Methods An animal model of VD was established through chronic hypoperfusion of cerebral blood flow of the forebrain in aging rats with permanent bilateral common carotid arteries occlusion. The rats were tested with a computerized shuttle-training case. The changes of cerebrovascular system were observed with digital subtraction angiography(DSA). The brain tissues were studied for choline acetyltransferase(ChAT) with immunohistochemistry. Results The congnitive function of rats was obviously reduced after 2 months of the chronic erebral hypoperfusion and became worse after 4 months of hypoperfusion. The distribution and number of the neutrons positive to ChAT-like immunoreaction in the CA1 sector of the hippocampus were more significantly reduced in the hypoperfused rats than in those of the control and the decrease of the positive neutrons was positively correlated to memory disorders. Conclusion Our rat model of VD can reliably simulate the clinical manifestation of VD in human being resulting from chronic hypoperfusion of cerebral blood flow. Damages of cholinergic neurons in the cortex of the frontal lobe and hippocampus are the morphological basis of impairment of the cognition function.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2000年第4期314-317,共4页
Journal of Third Military Medical University
基金
国家自然科学基金!资助项目(39770273)
关键词
血管性痴呆
动物模型
胆碱乙酰基
转移酶
s:vascular dementia
cognitive disorders
animal model
choline acetyltransferase
