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作 者:杨培润[1,2] 钱刚[1] 罗素元[1] 吴明松[1]
机构地区:[1]遵义医学院基础医学院,遵义563099 [2]安徽省颍上卫校,阜阳236200
出 处:《中国药物依赖性杂志》2012年第6期422-425,438,共5页Chinese Journal of Drug Dependence
基 金:教育部科学技术重点项目基金资助(206136)
摘 要:目的獉獉:探讨丁螺环酮治疗吗啡依赖戒断焦虑的细胞和分子机制。方法獉獉:66只雄性SD大鼠随机分为生理盐水对照组(对照组)、吗啡戒断焦虑组(模型组)、丁螺环酮治疗组(治疗组)。吗啡剂量递增皮下注射10 d自然戒断,于戒断1-3 d丁螺环酮灌胃治疗行高架十字迷宫实验后,取海马CA3区和杏仁核组织,用电镜体视学方法定量检测其各组突触的数密度(Nv)、面密度(Sv)、突触连接带平均面积(S),Western-blot技术检测其CaMKⅡ的含量和磷酸化水平。结果獉獉:与模型组比较,治疗组大鼠进入开放臂的次数和时间明显增加(P<0.01或P<0.05);海马CA3区和杏仁核突触的Nv和Sv显著降低、S增加(P<0.01或P<0.05),CaMKⅡ蛋白含量和β亚基磷酸化水平显著下调(P<0.01或P<0.05)。结论獉獉:逆转吗啡戒断焦虑大鼠海马、杏仁核突触结构的可塑性和CaMKⅡ分子的变化可能是丁螺环酮缓解吗啡戒断焦虑的重要细胞和分子机制。Objective:To explore the cellular and molecular mechanism of buspirone on anxiety in morphine withdrawal rats.Methods:The 66 male SD rats were randomly divided into three groups: the saline(control),the morphine(model),and the buspirone(treatment).Gradually increasing dosage of morphine with hypodermic injection is applied to validate the morphine dependence for 10 days before the elevated plus maze.Thus,the model rats are subjected to buspirone treatment for 1-3 d.The tissue of hippocampal region of CA3 and amygdala was harvested to test the scores of Nv(numerical density),Sv(surface density) and S(surface) with electron microscopy stereology.Total and phosphorylated levels of CaMKⅡ are detected by Western blotting.Results:Compared with the model group,the rats treated with buspirone had higher frequency and longer time in open arm(P0.01 or P0.05),and the lower values of Nv and Sv and higher score of S were observed in CA3 region of hippocampus and amygdale(P0.01 or P0.05).However,the decreased parameters of contents and the phosphorylase levels of CaMKⅡ were observed in the treated group(P0.01 or P0.05).Conclusion:Reversion of synaptic structural plasticity of hippocampus and amygdale and changed expression levels of CaMKⅡ may attribute the anxiolytic effects of buspirone in morphine withdrawal rats.
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