摘要
目的探讨慢性应激对大鼠行为及其脑内各部位PSD-95蛋白含量的影响。方法以慢性强迫游泳法制作单纯应激(慢性强迫游泳应激)和药物干预慢性应激(每次强迫游泳应激前皮下注射MK801)大鼠模型;用Western blotting蛋白质定量方法分别检测对照(无应激)组、单纯应激组和药物干预组大鼠的海马、前额叶皮质、基底节的PSD-95含量。结果在强迫游泳第14天时,单纯应激组大鼠的体质量增加明显慢于对照组和药物干预组;与对照组和药物干预组相比,单纯应激组大鼠的糖水消耗量明显减少,强迫游泳期间的不动时间显著延长;单纯应激组大鼠的海马、前额叶皮质的PSD-95含量均显著高于对照组和药物干预组,而基底节的PSD-95含量在3组之间差异无统计学意义。结论慢性强迫游泳大鼠是有价值的慢性应激模型;脑细胞内NMDA受体介导的信息传递功能亢进可能是这个动物模型的神经机制之一。
Objective To investigate the behavior effect and the contents change of PSD-95 in the rats' brain under chronic stress. Methods A pure stress(chronic forced swimming) and the MK801 intervention(injection MK801 before forced swimming) chronic stress model was established by chronic forced swimming.The PSD-95 contents in hippocampus,prefrontal and basal ganglia areas of the rats were measured by the method of Western blotting. Results At the 14th day of chronic forced swimming,the body weight gain was less in the pure stress group than the control or the MK801 intervention group,respectively.In the pure stress group,the value of sucrose consumption was less,the motionless time for forced swimming duration was longer,than the control or MK801 intervention group.The PSD-95 contents of hippocampus area,prefrontal area in pure stress group were significantly higher than that in control group and MK801 intervention group,but for the basal ganglia area there was no significant difference among the three groups. Conclusion Chronic forced swimming rat is an effective chronic stress model.Chronic forced swimming can enhance the message delivery function of the receptor-mediated NMDA within brain cells.
出处
《首都医科大学学报》
CAS
北大核心
2011年第6期820-824,共5页
Journal of Capital Medical University
基金
福建省自然科学基金计划资助项目(2010J01177)~~
关键词
慢性强迫游泳
慢性应激模型
突触后致密蛋白95
chronic forcing swimming
chronic stress model
postsynaptic density protein 95