摘要
目的 :观察拟血管性痴呆小鼠模型大脑皮层及海马细胞病理形态学的较长期演变。方法 :复制拟血管性痴呆小鼠模型 ,分别于术后 7d、15d、30d脑部取材 ,石蜡切片 ,HE与Nissl染色 ,对皮层及海马细胞病理形态学进行较长期动态观察。结果 :7d模型小鼠大脑皮质变薄 ,部分神经细胞核固缩 ,局限性神经元数目减少 ,出现筛网状结构 ,胶质细胞增生 ,15d、30d镜下与 7d基本相同。海马CA1区细胞脱失 ,随时间推移逐渐加重 ,至术后 30d ,海马CA1区细胞几乎完全脱失 ,胶质细胞大量增生 ,形成结节 ,CA2 、CA3 区细胞也严重脱失 ,呈现海马硬化。结论 :海马锥体细胞的迟发性坏死是缺血性脑血管病致痴呆的病理学基础。
AIM: To observe pathomorphological changes in cerebral cortex and hippocampus in the mouse with synthetic vascular dementia. METHODS: The synthetic vascular dementia model was produced in the mouse. Animals were killed 7 d, 15 d, and 30 d after the operation, brain tissues were removed and embedded in paraffin. Section of 8μm thickness were stained with hematoxylin-eosin(HE) and Nissl methods, and observed with light microscope. RESULTS: The cerebral cortex in the mouse became thinner on the seventh day, karyopyknosis in partial nervous cells was formed, the number of local neurons was reduced, sieve structure was observed, and glial cells proliferated, with the similar results 15 d and 30 d after operation. Model mouses hippocampal cells in CA 1 area were reduced and almost disappeared 30 d after operation. At the same time, glial cells were abundantly proliferated, tubercles were formed. Cells in CA 2, CA 3 area were also reduced and hippocampal sclerosis occurred. CONCLUSION: Delayed necrosis of hippocampal pyramidal cells may be the pathological basis of ischemia cerebral vascular dementia.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第11期1214-1216,共3页
Chinese Journal of Pathophysiology
基金
河北省卫生厅资助项目!(No .990 12 )
关键词
血管性痴呆
大脑皮层
细胞病理形态学
Dementia, vascular
Cerebral cortex
Hippocampus
Pyramidal cells
Necrosis
