杏仁核脑区硫化氢对创伤后应激障碍模型大鼠抑郁样行为的影响

发布时间：2018-04-13 01:09

本文选题：硫化氢 + 创伤后应激障碍　；参考：《中国病理生理杂志》2017年06期

【摘要】：目的:探讨创伤后应激障碍(posttraumatic stress disorder,PTSD)大鼠抑郁样行为改变及杏仁核内胱硫醚β-合成酶(cystathionineβ-synthase,CBS)/硫化氢(hydrogen sulfide,H_2S)水平的变化,并研究补充H_2S对大鼠抑郁样行为的作用及机制。方法:应用连续单一应激方案制备PTSD动物模型,用强迫游泳实验和糖水偏好实验检测大鼠抑郁样行为,用Western blot技术和亚甲基蓝法检测杏仁核CBS/H_2S体系含量,用整体细胞外电生理方法记录杏仁核神经元放电情况。结果:与正常对照组比较,PTSD组大鼠强迫游泳不动时间显著延长(P0.01),糖水偏好率显著降低(P0.01);杏仁核脑区的CBS/H_2S体系含量显著降低(P0.01)。与PTSD组比较,PTSD+硫氢化钠组大鼠强迫游泳不动时间显著减少(P0.01),糖水偏好率显著升高(P0.01)。微量压力注射L-半胱氨酸使杏仁核神经元自发放电频率显著升高(P0.01)。结论:PTSD大鼠通过抑制杏仁核CBS/H_2S体系导致抑郁样行为加重。H_2S拮抗PTSD大鼠抑郁样行为的机制可能与其增加杏仁核神经元放电频率和兴奋性有关。
[Abstract]:Objective: to investigate the changes of depressive behavior and the level of cystathionine 尾 -synthase in amygdala of posttraumatic stress disorder (PTSD) rats, and to study the effect and mechanism of H2S supplementation on depressive behavior in rats.Methods: PTSD animal model was established by continuous single stress program. The depressive behavior of rats was measured by forced swimming test and sugar water preference test. The content of CBS/H_2S system in amygdala was detected by Western blot technique and methylene blue method.The discharge of amygdala neurons was recorded by the whole extracellular electrophysiological method.Results: compared with the control group, the immobility time of forced swimming in PTSD group was significantly prolonged, the preference rate of sugar and water decreased significantly, and the content of CBS/H_2S system in the amygdaloid nucleus decreased significantly.Compared with PTSD group, the immobility time of forced swimming in PTSD group was significantly reduced, and the preference rate of sugar water was increased significantly (P 0.01).Micropressure injection of L-cysteine increased the spontaneous discharge frequency of amygdaloid neurons significantly (P 0.01).Conclusion the mechanism of inhibition of amygdala CBS/H_2S system induced depression like behavior in PTSD rats may be related to the increase of firing frequency and excitability of amygdaloid neurons.
【作者单位】：滨州医学院基础医学院生理学教研室;滨州医学院病理学教研室;滨州医学院药理学教研室;
【基金】：山东省自然科学基金资助项目(No.ZR2013HL009;No.BS2015YY036;No.BS2014YY049) 烟台市科技发展计划项目(No.2012ZH248;No.2015ZH085)
【分类号】：R-332;R749.5

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