摘要
目的观察创伤后应激障碍(PTSD)大鼠海马神经元Ca2+信号及钙调蛋白(CaM)的表达变化,探讨PTSD行为异常的神经生物学机制。方法采用国际认定的无连续单一应激(SPS)方法刺激建立大鼠PTSD模型。成年健康雄性Wistar大鼠60只,随机分为SPS模型的12h、1d、4d、7d组及正常对照组,采用荧光探针标记法、免疫组织化学、免疫印迹和RT-PCR法检测Ca2+含量和CaM的表达变化。结果SPS刺激后大鼠海马神经元内游离Ca2+浓度(nmol/L)于12h内升高,24h增至顶峰,7d恢复正常。CaM的表达于SPS刺激后1d表达最多,之后渐趋下降。结论海马Ca2+信号调控与CaM的表达变化可能是PTSD大鼠情感行为异常的重要病理生理基础之一。
Objective To observe the changes of intracellular free calcium and the expression of CaM in the hippocampal neurons of posttraumatic stress disorder （PTSD） rats and to further investigate the neurobiological mechanisms. Methods The SPS-method was used to set up the rat PTSD models. A total of sixty male Wistar rats were randomly divided into 12 hours, 1 day, 4 days, 7 days groups of SPS and normal control group. The intracellular free calcium was examined by fluorescence spectrophotometer. The expression of CaM was detected by using immunohistochemistry, Western blotting and RT-PCR. Results The intracellular free calcium level in the hippocampus of experimental rats was markedly increased 12 hours after SPS stimulation, and reached the peak after 1 day, then gradually decreased to normal level after 7 days. The expression of CaM in the hippocampus lday, after SPS was also the highest and then gradually decreased. Conclusion The lasting dysfunction＇ of Ca2＋ /CaM signaling cascades in hippocampal may play important roles in the pathogenesis of PTSD rats.
出处
《解剖学报》
CAS
CSCD
北大核心
2009年第6期877-880,共4页
Acta Anatomica Sinica
基金
国家自然科学基金资助项目(30600341)
