一种Alzheimer痴呆小鼠模型的建立
投稿时间:2009-12-08  修订日期:2009-12-16  点此下载全文
引用本文:王清华,徐如祥.一种Alzheimer痴呆小鼠模型的建立[J].医学研究杂志,2010,39(4):54-56
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作者单位
王清华 南方医科大学珠江医院神经外科 
徐如祥 南方医科大学珠江医院神经外科 
中文摘要:目的建立Alzheimer痴呆(Alzheimer dementia, AD)小鼠模型。方法C57BL/6小鼠基底巨细胞核(NBM)注射Ibotenic 酸制成AD模型。8周后应用8方向迷宫评价小鼠痴呆程度,应用免疫组织化学染色观察NBM和脑皮质胆碱能系统和β-淀粉样蛋白表达改变。结果NBM内胆碱能神经元明显减少,5-羟色胺(5-HT)神经元和GABA神经元轻度减少。同侧额、顶叶皮质内胆碱能神经纤维显著减少,5-HT神经轴突轻度减少,伴大量β-淀粉样蛋白表达,GABA神经元则无明显变化。NBM毁损小鼠的工作记忆错误显著升高,小鼠的近事记忆明显损害。结论NBM注射Ibotenic 酸能建立一种可靠的AD小鼠模型。
中文关键词:基底巨细胞核 胆碱能神经元 Alzheimer痴呆模型 小鼠
 
Establishment of a Mouse Model of Alzheimer Dementia
Abstract:AbstractObjectiveTo establish a Alzheimer dementia(AD) model in mice. MethodsThe C57BL/6 mice were lesioned with ibotenic acid in Nucleus basalis of Meynert(NBM). Behavioral tests by eight-arm radial maze were conducted 8 weeks, and immunohistochemical staining of choline acetyltransferase(ChAT), serotonin(5-HT), GAD(GABA), amyloid-βprotein (AP) was conducted 12 weeks after NBM lesioning. ResultsIn NBM lesioned mice, the ChAT-positive neurons, serotonin-positive neurons, and GAD-positive neurons in right NBM reduced, and ChAT-positive neurons reduced most evidently. At the same time, the ChAT-positive fibers in prefrontal and parietal cortices decreased significantly, serotonin-positive axons slightly, accompanied by heavily AP co-expression. On the contrary, there was no change of GAD-positive neurons in cortex. The working memory error increased significantly.ConclusionIbotenic acid lesioning in NBM can provide as a model of AD in that it produces deafferentation of cholinergic system and recent memory disruption.
keywords:Nucleus basalis of meynert  Cholinergic neuron  Alzheimer dementia model  Mouse
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