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Possible antidepressant effects and mechanism of electroacupuncture in behaviors and hippocampal synaptic plasticity in a depression rat model

机译：抑郁症大鼠模型中行为和海马突触可塑性的可能抗抑郁作用和机制

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Increasing evidences show that hippocampal synaptic plasticity plays a crucial role in the pathogenesis of depression. The objective of this study was to determine whether electroacupuncture (EA) in the Wistar Kyoto (WKY) rat model of depression would exert antidepressant effects and whether this effect would be associated with changes in hippocampal synaptic plasticity. Male WKY rats were randomly divided into three groups (EA, sham EA, and blank control); Wister rats were used as normal control group. Treatment with EA was performed at Baihui (GV20) and Yintang (EX-HN3) once daily for 3 weeks. Forced swimming test (FST), open field test (OFT), and Morris water maze (MWM) were evaluated after 21-day intervention. Longterm potentiation (LTP) was evoked at Schaffer collateral-CA1 synapses in hippocampal slices in vitro. EA treatment significantly reduced immobility time in FST. MWM test showed a significant downward trend in escape latency time from the second to fifth days of experiment, and a higher frequency of crossing the missing quadrant platform in normal control and EA vs other groups. Impaired LIT was detected in Schaffer collateral-CA1 synapses in blank control and sham EA groups. In the western blot, the expression of GluN2B showed significant increase in EA vs sham EA and blank control groups. EA was able to improve depression-like behaviors and reverse the impairment of LIT, which were likely mediated by GluN2B in the hippocampus. (C) 2015 Elsevier B.V. All rights reserved.
机译：越来越多的证据表明，海马突触可塑性在抑郁症的发病机理中起着至关重要的作用。这项研究的目的是确定Wistar Kyoto（WKY）大鼠抑郁模型中的电针（EA）是否会发挥抗抑郁作用，以及该作用是否与海马突触可塑性的变化有关。将雄性WKY大鼠随机分为三组（EA，假EA和空白对照组）。雄性大鼠作为正常对照组。每天一次在百会（GV20）和银塘（EX-HN3）进行EA治疗，持续3周。在21天的干预后，评估了强迫游泳测试（FST），露天测试（OFT）和莫里斯水迷宫（MWM）。体外海马切片中的沙弗侧支CA1突触引起长期增强（LTP）。 EA治疗显着减少了FST的不动时间。 MWM测试显示，从实验的第二天到第五天，逃避潜伏时间有明显的下降趋势，而正常对照组和EA组与其他组相比，越过缺失象限平台的频率更高。在空白对照组和假EA组的Schaffer侧支CA1突触中检测到LIT受损。在蛋白质印迹中，与假EA和空白对照组相比，EA中GluN2B的表达显着增加。 EA能够改善抑郁症样行为并逆转LIT损伤，这可能是由海马中的GluN2B介导的。 （C）2015 Elsevier B.V.保留所有权利。

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