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毁损Meynert基底核造成皮层及海马的乙酰胆硷酯酶减少行为学和形态学研究(英文)
引用本文:李琳,陈晋原,乔健天.毁损Meynert基底核造成皮层及海马的乙酰胆硷酯酶减少行为学和形态学研究(英文)[J].神经解剖学杂志,1999(2).
作者姓名:李琳  陈晋原  乔健天
作者单位:山西医科大学神经生物学研究室!太原030001
摘    要:本研究通过毁损M eynert基底核(nbM )建立Alzheim er氏病(AD)动物模型。用乙酰胆硷酯酶(AChE)细胞化学方法对模型动物大脑皮层及海马进行反应,评价AChE 与AD 之间可能存在的关系。将48 只大鼠分成对照组及实验组,用Morris 水迷宫(MW M )测定行为学变化。在实验组,以局部注射海人藻酸的方法毁损nbM 。术后7 d,再次检测其行为学变化。存活不同时间后,用AChE 酶细胞化学技术染色脑切片,用图象分析系统测算海马层AChE阳性神经元及纤维的体积密度。结果显示,毁损nbM 鼠皮质及海马的AChE阳性神经元纤维明显减少,其特征为片层结构缺失。这些变化在毁损nbM 鼠3~4 个月及9~10 个月组间无显著差异。本研究证明,毁损nbM 出现的AChE减少与AD 的发生关系密切,且与同一动物模型β 淀粉样蛋白及τ蛋白过度表达在时间上一致,后者是AD 病人的特征。

关 键 词:AChE  大脑皮质  海马  Meynert基底核毁损大鼠

DECREASE OF ACETYLCHOLINESTERASE IN CEREBRAL CORTEX AND HIPPOCAMPUS BY LESION OF NUCLEUS BASALIS OF MEYNERT IN RATS: A BEHAVIORAL AND MORPHOLOGICAL STUDY
Li Lin,Chen Jinyuan,Qiao Jiantian.DECREASE OF ACETYLCHOLINESTERASE IN CEREBRAL CORTEX AND HIPPOCAMPUS BY LESION OF NUCLEUS BASALIS OF MEYNERT IN RATS: A BEHAVIORAL AND MORPHOLOGICAL STUDY[J].Chinese Journal of Neuroanatomy,1999(2).
Authors:Li Lin  Chen Jinyuan  Qiao Jiantian
Abstract:To evaluate the possible relationship between acetylcholinesterase(AChE) and Alzheimer's disease(AD), the enzymatic cytochemical staining for AChE was carried out on sections of cerebral cortex and hippocampus of rats after lesion of nucleus basalis of Meynert(nbM). 48 rats were divided into control and experimental groups and behavioral performance was examined first by Morris water maze(MWM). The nbM were destroyed by local injection of kainic acid in experimental animals. Seven days after operation, behavioral changes were examined again. After different time of survival, brain sections were stained with AChE enzymatic cytochemical technique and the volume density of AChE positive neurons and fibers in hippocampus and cerebral cortex were measured by an image processing system. Results: AChE positive neurons and fibers of nbM lesioned rats revealed a strong depletion in the neocortex and hippocampus; the loss of the characteristic lamination of neural elements was also existed in these areas. These changes appeared to be permanent and showed no significant differences when examined 3~4 months or 9~10 months after nbM lesion. Conclusions: The lesion of nbM induces AChE depletion which coincides with the overexpression of β AP and τ protein characteristic of AD patients.
Keywords:AChE  cerebral cortex  hippocampus  nucleus basalis of Meynery  lesioned rat
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