摘要
目的检测分子伴侣钙网蛋白(CRT)在创伤后应激障碍(PTSD)大鼠海马神经元中表达的变化,探讨CRT对PTSD大鼠海马神经元内Ca2+信号的调节,为研究PTSD海马记忆异常的发病机制提供依据。方法采用单一延长应激(SPS)方法刺激大鼠建立PTSD大鼠模型,成年健康雄性Wistar大鼠随机分为SPS1 d、4 d、7 d组和正常对照组。采用免疫组织化学、免疫印迹和逆转录聚合酶链反应检测大鼠海马神经元CRT的表达变化;用荧光探针标记法检测大鼠海马神经细胞内游离Ca2+浓度变化。结果 SPS刺激后大鼠海马神经元CRT的表达于刺激后7 d最多;细胞内游离Ca2+浓度于1 d增至顶峰,之后逐渐下降。结论PTSD致内质网应激、海马神经元钙超载、内质网分子伴侣CRT表达上调、激活未折叠蛋白反应,可导致细胞凋亡,这可能是PTSD大鼠海马记忆异常的病理生理基础。
Objective To investigate the expression of molecular chaperone calreticulin （CRT） on the hippocmnpus in rat post-traumatic stress disoirter （PTSD） model,and discuss the regulation of CRT on Ca2＋ in hippocampus of PTSD rats,so as to provide an experiment basis for pathogenesis of memory anomaly in PTSD rats. Methods The rat PTSD models were established by using method of single-prolonged stress （ SPS ）. Samples were collected from male Wistar rats before or 1,4,7 days after exposure to SPS. The expression of CRT was detected by using immunohistoehemistry, Western blot and RT-PCR. The intracellular free calcium was examined by fluorescence spectrophotometer. Results The expression of CRT in the hippocampus increased ＇after SPS stimulation, and reached the peak at SPS 4 d. The intmcellular free calcium level in the hippcw, ampus increased,and reached the peak at SPS 1 d,then gradually decreased. Conclusion PTSD can in- duce cell apoptosis through endoplasmic retieulum stress, calcium overload, up-regulated expression of CRT, and activation of unfolded protein response, which could be the pathogenesis basis on memory anomaly in PTSD rats.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2012年第12期1057-1059,1064,共4页
Journal of China Medical University
基金
国家自然科学基金资助项目(81171282)
