Electroacupuncture improves synaptic plasticity by regulating the 5-HT1A receptor in hippocampus of rats with chronic unpredictable mild stress
Electroacupuncture improves synaptic plasticity by regulating the 5-HT1A receptor in hippocampus of rats with chronic unpredictable mild stress
复制标题
电针通过调节慢性不可预测轻度应激大鼠海马5-HT1A受体改善突触可塑性
DOI：
10.1177/0300060520918419
复制
发表时间：
2020-05-01
影响因子：
1.6
通讯作者：
Zhong, Zheng
中科院分区：
文献类型：
--
作者：
Chen, Lixing;Yao, Zengyu;Zhong, Zheng
目的探讨电针（EA）对大鼠慢性不可预测轻度应激（CUMS）的抗抑郁作用，以及电针对海马神经元、突触形态和5-羟色胺（HT）受体表达的影响。方法40只成年雄性Wistar大鼠随机分为正常对照组、CUMS组、EA组和帕罗西汀组。CUMS建模21天，干预14天：EA组大鼠GV20、GV29穴位刺激，每日30分钟；帕罗西汀组大鼠每日给予帕罗西汀。使用行为测试、透射电镜、免疫印迹和实时定量聚合酶链反应来评估干预的效果。结果EA治疗逆转了CUMS模型大鼠的行为改变；改善了海马神经元细胞器和突触结构的病理改变，上调了5-HT1A受体蛋白和mRNA的表达水平。各组间5-HT1B受体蛋白及mRNA表达水平无显著差异。结论EA治疗可减轻CUMS大鼠抑郁样症状。其潜在机制可能包括促进5-HT1A受体mRNA和蛋白的表达，从而改善海马突触可塑性。
Objectives To investigate the antidepressant effects of electroacupuncture (EA) on chronic unpredictable mild stress (CUMS) in rats, as well as the effects of EA on hippocampal neurons, synaptic morphology, and 5-hydroxytryptamine (HT) receptor expression. Methods Forty adult male Wistar rats were randomly divided into normal control, CUMS, EA, and paroxetine groups. CUMS modeling was performed for 21 days, followed by 14 days of intervention: rats in the EA group underwent stimulation of GV20 and GV29 acupuncture points for 30 minutes daily; rats in the paroxetine group were administered paroxetine daily. Behavioral tests, transmission electron microscopy, western blotting, and real-time quantitative polymerase chain reaction were used to evaluate the effects of the intervention. Results EA treatment reversed the behavioral changes observed in rats due to CUMS modeling; it also improved the pathological changes in organelles and synaptic structures of hippocampal neurons, and upregulated the protein and mRNA expression levels of 5-HT1A receptor. There were no significant differences in 5-HT1B receptor protein and mRNA expression levels among the groups. Conclusions EA treatment can alleviate depression-like symptoms in CUMS rats. The underlying mechanism may include promoting the expression of 5-HT1A receptor mRNA and protein, thereby improving synaptic plasticity in the hippocampus.