摘要
目的:研究阿尔茨海默病(AD)样大鼠模型海马内突触后致密物-95(PSD-95)表达与学习记忆损伤的元素。方法:健康成年雄性SD大鼠随机分为正常对照组、模型对照组和AD模型组。AD样大鼠模型的建立采用Aβ1-40/Al Cl3双干预法。采用Morris水迷宫和跳台实验检测大鼠的学习记忆能力,采用刚果红染色和尼氏染色观察大鼠海马病理变化,采用免疫印迹的方法检测大鼠海马PSD-95的表达情况。结果:与正常对照组和模型对照组相比,AD模型组大鼠Morris水迷宫逃避潜伏期明显延长(P<0.05),跳台实验的反应时间、基础错误次数和错误次数均增加,潜伏期缩短(P<0.05)。AD模型组大鼠海马可观察到明显的病理改变,正常对照组和模型对照组中则观察不到。与正常对照组和模型对照组相比,AD模型组大鼠海马PSD-95的表达明显降低(P<0.05)。结论:PSD-95在AD样大鼠海马表现为病理性低表达,并且这种病理性低表达很可能与AD样学习记忆损伤存在联系。
Objective: To study relatianship of PSD-95 expression in hippocampus of Alzheimer's disease-like rats and learning and memory functions. Methods: The healthy aged male SD rats were randomly devided into normal control,model control and AD-like model groups. Aβ1-40 and Al Cl3 were used to establish AD-like model. Morris water maze test and step-down test were used to detect the learning and memory function of rats,Congo red and Nissl staning were used to observe the pathology of rats' hippocampus and Western Blotting was used to detect the expression of PSD-95 in each group. Results: Compared with normal control and model control,the water maze test escape latency of AD model rats was longer( P〈 0. 05),the test learning time,basal number of errors and number of errors of step-down were increased and the latency period was decreased( P〈 0. 05). Pathologit changes could be observed in rats' hippocampus,not in normal control group and model control group. Compared with normal control group and model control group,the expression of PSD-95 in AD model group was decreased( P〈 0. 05). Conclusion: Expression of PSD-95 was decreased in AD-like rat hippocampus. This decreased expression might involve in the AD-like learning and memory deficits.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2016年第2期217-222,共6页
Chinese Journal of Neuroanatomy
基金
杭州市科技计划重点专科专项课题(20120533Q41)
徐州医学院院长基金(2012KJZ08)