Zhang Kun, Liu Ran, Zhang Jingruo, Wei Xifang, Gao Yuan, Ma Wen, Li Yijing, Cai Wa, Shen Weidong
Department of Acupuncture, Shuguang Hospital affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Institute of Acupuncture and Anesthesia, Shuguang Hospital affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Evid Based Complement Alternat Med. 2021 Nov 3;2021:2146001. doi: 10.1155/2021/2146001. eCollection 2021.
Hippocampal synaptic plasticity during the pathological process of depression has received increasing attention. Hippocampal neuron atrophy and the reduction in synaptic density induced by chronic stress are important pathological mechanisms of depression. Electroacupuncture (EA) exerts beneficial effects on depression, but the mechanism is unclear. This study explored the effect of EA on synaptic plasticity and the potential mechanism.
Forty-eight SD rats were randomly divided into the control, chronic unpredictable mild stress (CUMS), EA, and fluoxetine (FLX) groups, and each group consisted of 12 rats. The sucrose preference test, open field test, and forced swimming test were used for the evaluation of depression-like behaviour, and Golgi and Nissl staining were used for the assessment of synaptic plasticity. Western blotting and immunofluorescence were conducted to detect proteins related to synaptic plasticity and to determine their effects on signalling pathways.
We found that CUMS led to depression-like behaviours, including a reduced preference for sucrose, a prolonged immobility time, and reduced exploration activity. The dendritic spine densities and neuron numbers and the protein levels of MAP-2, PSD-95, and SYN were decreased in the hippocampi of rats with CUMS-induced depression, and these trends were reversed by EA. The molecular mechanism regulating this plasticity may involve the GluN2B/CaMKII/CREB signalling pathway.
These results suggest that EA can improve depression-like behaviour and hippocampal plasticity induced by CUMS, and the mechanism may be related to the GluN2B/CaMKII/CREB pathway.
抑郁症病理过程中的海马突触可塑性受到越来越多的关注。慢性应激诱导的海马神经元萎缩和突触密度降低是抑郁症的重要病理机制。电针（EA）对抑郁症有有益作用，但其机制尚不清楚。本研究探讨了EA对突触可塑性的影响及潜在机制。
将48只SD大鼠随机分为对照组、慢性不可预测轻度应激（CUMS）组、EA组和氟西汀（FLX）组，每组12只。采用蔗糖偏好试验、旷场试验和强迫游泳试验评估抑郁样行为，采用高尔基染色和尼氏染色评估突触可塑性。进行蛋白质免疫印迹和免疫荧光检测与突触可塑性相关的蛋白质，并确定它们对信号通路的影响。
我们发现CUMS导致抑郁样行为，包括蔗糖偏好降低、不动时间延长和探索活动减少。CUMS诱导的抑郁大鼠海马中的树突棘密度、神经元数量以及MAP-2、PSD-95和SYN的蛋白质水平降低，而EA可逆转这些趋势。调节这种可塑性的分子机制可能涉及GluN2B/CaMKII/CREB信号通路。
这些结果表明，EA可改善CUMS诱导的抑郁样行为和海马可塑性，其机制可能与GluN2B/CaMKII/CREB通路有关。
