摘要
为了探讨神经生长因子(NGF)预处理对拟Alzheimer病(AD)模型大鼠海马CA1区和顶叶皮层内神经原纤维缠结(NFT)和胆碱乙酰基转移酶(ChAT)表达的影响,本研究将动物分为拟AD组和NGF预处理组。将冈田酸(OA)微量注射至拟AD组大鼠海马CA1区(0.4mmol/L,0.5ml/次;隔天1次,共7次)建立拟AD大鼠模型,NGF预处理组于制模前10d将NGF(0.1mg/ml,5ml/次;隔天1次,共10次)注射至侧脑室。通过Morris水迷宫观察上述大鼠的行为学变化,分别用改进的Bielschowsky染色和免疫组化法观察海马及顶叶皮层内NFT和ChAT表达的变化。结果显示:拟AD模型组大鼠出现认知、学习记忆能力减退,海马CA1区及顶叶皮层出现较多的NFT,而ChAT表达减少;NGF预处理组大鼠的上述症状明显改善。这些结果提示OA的神经毒性可以导致拟AD模型大鼠的学习记忆能力降低,并且出现胆碱能神经元损伤和功能低下;NGF预处理可以显著改善拟AD模型大鼠的学习记忆能力,抑制海马CA1区和顶叶皮层内NFT的形成,减轻对胆碱能神经元的损伤。
To investigate the effects of nerve growth factor （NGF） pretreatment on both neurofibrillary tangles （NFT） and choline acetyltransferase （CHAT） expression in the hippocampal CA1 region and parietal cortex in the Alzheimer＇s Disease （AD）-like model rats. The rats were divided into AD-like group and NGF-pretreatment group. The AD-like animal model was induced by okadaic acid （OA） injected into hippocampal CA1 region （0.4 mmol/L, 0.5 ml/time; one time 2 days for 7 times）. For the NGF-pretreatment group, NGF was injected into the lateral ventricle of the brain 10 days before OA was injected to establish the AD-like animal model （0.1 mg/ml, 5 ml/time; one time 2 days for 10 times）. The behavior changes of rats were observed by Morris water maze. Then, the changes of NIT formation and ChAT expression in the hippocampus and parietal cortex were observed by Bielschowsky staining and immunohistochemical method, respectively. The results showed that the impairment learning and the memory deficits in the AD-like model rats were observed; there were more NFTs, but the ChAT expression was decreased in the hippocampus and parietal cortex. However, in the NGF-pretreated group, the abovementioned symptoms were improved obviously. These results suggest that OA＇s neurotoxicity can cause degrading of the learning and memory capability, and result in cholinergic neuron damage and function deficit. NGF pretreatment can significantly improve the learning and memory capabilities of the AD-like model rats, inhibit the formation of NFT in the hippocampal CA1 region and parietal cortex, and lessen damage of cholinergic neurons.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2007年第6期655-661,共7页
Chinese Journal of Neuroanatomy
基金
贵州省优秀科技教育人才省长专业基金(S2001-3)资助项目
