TY -非盟的徐小红盟——郑,彭盟——赵,红岩盟歌,Bailin AU -王,《PY - 2020 DA - 2020/08/21 TI -效应的电针刺激对小鼠睡眠Deprivation-Induced类似抑郁行为GV20 SP - 7481813六世- 2020 AB -越来越多的证据表明睡眠剥夺(S-Dep)是一个萧条的关键风险因素。电针刺激(EA)治疗改善创伤后应激障碍的报道——(PSTD)像行为和提高海马神经发生。然而,EA治疗是否有益影响S-Dep-induced类似抑郁的行为仍然是未知的。在目前的研究中,我们关注是否EA Baihui (GV20)可以改善S-Dep恶化影响的老鼠。小鼠随机分为正常、S-Dep S-Dep + EA, S-Dep +假EA组。认知行为测试和体外试验进行了分别以避免行为测试对突触传递和蛋白质表达的影响。类似抑郁的行为是由强迫游泳试验(置),尾部测试(TST)和莫里斯水迷宫(微波加工)。神经发生被BrdU、克莱斯勒和NeuN免疫荧光染色。体外长期势差是探测到高频刺激(HFS)在海马切片谢弗collateral-CA1突触。脑源性嗜神经因子(BDNF)和原肌球蛋白受体激酶B (TrkB)蛋白表达水平受到免疫印迹的化验。 Our results indicated that D-Sep mice demonstrated depression-like behaviors determined by prolonged immobility duration in FST and TST; D-Sep mice also manifested spatial memory retention deficit in MWM. Furthermore, EA treatment ameliorated D-Sep-induced depression-like behaviors and spatial memory retention deficit. Mechanically, EA treatment alleviated neuron progenitor cell proliferation and differentiation, ameliorated the field excitatory postsynaptic potentials (fEPSPs) slope impaired by S-Dep, and elevated BDNF/TrkB protein expression. Taken together, our data suggested that EA treatment has a protective effect on S-Dep-induced depression-like behavior and cognitive impairment, which may be through regulating BDNF/TrkB protein expression. SN - 1741-427X UR - https://doi.org/10.1155/2020/7481813 DO - 10.1155/2020/7481813 JF - Evidence-Based Complementary and Alternative Medicine PB - Hindawi KW - ER -