摘要
目的研究慢性不可预知性应激配合孤养对大鼠学习记忆能力和微管相关蛋白-2(MAP-2)表达的影响,为揭示慢性心理应激损伤大鼠海马功能的可能机制提供参考依据。方法把16只Wistar大鼠随机分为对照组、应激组。采用脑立体定位神经电生理方法测定大鼠海马齿状回长时程增强效应(long-term potentiation,LTP),以评定慢性应激对认知功能的影响,并以高频刺激前群峰电位幅值作为100%;采用western boltting检测海马微管相关蛋白质-2的表达变化。结果经过21 d不可预知性应激以后,高频刺激20 min,应激组海马齿状回的群峰电位幅值为191.3%,显著低于对照组〔239.1%(P<0.05)〕;在高频刺激60min内的不同时间点上,应激组海马齿状回的群峰电位幅值均显著低于对照组(P<0.05),与对照组比较,应激组的海马MAP-2蛋白表达(灰度值0.37)显著下调,差异有显著性(P<0.01)。结论慢性不可预知性心理应激过程使大鼠海马相关认知功能显著降低,其作用机制可能与应激导致海马MAP-2表达下调、神经元结构损伤和改变有关。
Objective To study the effect of chronic unpredictable mild stress(CUMS)and isolated-living on the cognitive function and expression of hippocampal microtubule associatied protein-2(MAP-2) in rats, so as to provide the basis for exploring the possible mechanism of CUMS induced-damage to hippocampal cognitive function. Methods Sixteen male Wistar rats were randomly divided into normal control group and stress group. Long-term potentiation(LTP) was induced in hippocampal dentate gyrus(DG)by high-frequency stimulation(HFS) to observe the cognitive function of the rats. The change of MAP-2 expression was examined by Western bohting. Results After CUMS stimulation for 21 days, the amplitude of population spike(PS)within 60 min HFS was markedly lower in stress group than in control group, e.g. the amplitude of PS at 20 min was 191.3 % for stress group, and 239.1% for control group( P 〈 0.05). The ex- pression of hippocampus MAP-2 in the stress group was also obviously down-regulated( P 〈 0.01 ). Conclusion Chronic unpredictable mild stress intensively attenuates the cognitive function in rat hippocampus, which may be related with the down-reaulation of MAP-2 and the damage of neuronal structure induced by stress.
出处
《解放军预防医学杂志》
CAS
2012年第4期239-242,共4页
Journal of Preventive Medicine of Chinese People's Liberation Army