PTSD样行为异常大鼠杏仁核Ca^2＋/CaM的改变

目的观察创伤后应激障碍（PTSD）样行为异常大鼠杏仁核细胞内Ca^2＋信号及Ca M（钙调蛋白）表达变化,有望揭示PTSD的部分发病机制。方法成年健康雄性Wistar大鼠60只,随机分为连续单一刺激（single prolonged stress,SPS）模型的12h、1d、4d、7d、14d组及正常对照组,采用荧光探针标记法、免疫组化、Western blott等方法,检测PTSD样行为异常大鼠杏仁核神经元游离Ca^2＋含量和钙调蛋白（Ca M）的表达变化。结果SPS刺激后大鼠杏仁核神经元游离Ca^2＋浓度（nmol/L）于12h内升高,24h增至顶峰,4d开始下降,14d恢复正常。CaM的表达于SPS刺激后4d表达最多,之后渐趋下降。结论杏仁核Ca^2＋信号调控与Ca M表达变化,可能与PTSD样大鼠恐惧增强的发病机制相关。

EXPRESSIONS OF CA2+AND CALMODULIN IN AMYGDALA OF RATS WITH POSTTRAUMIC STRESS DISORDER-LIKE BEHAVIOR

Objective To observe the changes of intracellular free calcium and the expression of CaM in amygdala neurons of PTSD rats to reveal part of the pathogensis. Methods A total of 60 male Wistar rats were randomly divided into 12h, ld, 4d, 7d and 14d groups of SPS and a normal control group. The intracellular free calcium was examined by fluorescence spectrophotometer. The expression of CaM was detected by using immunohistochemistry and Western blot. Results The intracellular free calcium level in the amygdala of experimental rats was markedly increased than the of the control group 12h after SPS stimulation, and reached the peak after 1 day. It was still elevated 4 days after stimulation, and then gradually decreased to normal level. The expression of CaM in the amygdala was strongest 4 days after SPS and then gradually decreased. Conclusion The lasting dysfunction of Ca^2＋/CaM signaling cascades in amygdala may be related to the pathogenesis of enhanced fear in PTSD rats.