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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 the expression of PSD-95 and learning and memory impairment in the hippocampus of Alzheimer’s disease (AD) -like rat model. Methods: Healthy adult male Sprague-Dawley rats were randomly divided into normal control group, model control group and AD model group. AD-like rat model was established by Aβ1-40 / Al Cl3 double intervention method. Morris water maze and jumping test were used to detect the learning and memory abilities of rats. The hippocampal pathological changes were observed by Congo red staining and Nissl’s staining. The expression of PSD-95 in hippocampus was detected by Western blot. Results: Compared with the normal control group and the model control group, the escape latency of Morris water maze was significantly prolonged in AD model rats (P <0.05), and the reaction time, the number of basic errors and the number of errors in jumping test were increased and the incubation period was shortened (P <0.05). Alzheimer’s disease rats showed obvious pathological changes in hippocampus of AD model group, but not in normal control group and model control group. Compared with normal control group and model control group, the expression of PSD-95 in hippocampus of AD model group was significantly decreased (P <0.05). CONCLUSIONS: PSD-95 is pathologically poorly expressed in the hippocampus of AD-like rats, and this pathological low expression is likely to be associated with AD-like learning and memory impairment.