Electroacupuncture alleviates PTSD-like behaviors by modulating hippocampal synaptic plasticity via Wnt/β-catenin signaling pathway

被引:6
作者
Lv, Tao [1 ,2 ]
Wang, Min [1 ]
Zheng, He-Sheng [1 ,2 ]
Yang, Fan [1 ,3 ]
Yang, Le [3 ]
Zhao, Ming -Gao [3 ]
Liu, Shui-Bing [1 ]
Zhang, Kun [1 ]
Liu, Rui [4 ]
Wu, Yu-Mei [1 ,2 ]
机构
[1] Air Force Med Univ, Sch Pharm, Dept Pharmacol, Xian 710032, Shaanxi, Peoples R China
[2] Shaanxi Univ Chinese Med, Dept Acupuncture moxibust massage, Xian 712000, Shaanxi, Peoples R China
[3] Air Force Med Univ, Tangdu Hosp, Dept Pharm, Xian 710038, Shaanxi, Peoples R China
[4] Air Force Med Univ, Tangdu Hosp, Dept Rehabil Med, Xian 710038, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Post-traumatic stress disorder; Electroacupuncture; Hippocampus; Synaptic plasticity; Wnt/beta-catenin signaling pathway; STRESS; RESILIENCE; PROMOTES; ROLES; MODEL;
D O I
10.1016/j.brainresbull.2023.110734
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Abnormalities in hippocampal synaptic plasticity contribute to the pathogenesis of post-traumatic stress disorder (PTSD). The Wnt/beta-catenin signaling pathway is critical for the regulation of synaptic plasticity. PTSD symptoms can be alleviated by correcting impaired neural plasticity in the hippocampus (Hipp). Electroacupuncture (EA) has a therapeutic effect by relieving PTSD-like behaviors. However, little is known about whether the Wnt/ beta-catenin pathway is involved in EA-mediated improvements of PTSD symptoms. In this study, we found that enhanced single prolonged stress (ESPS)-induced PTSD led to abnormal neural plasticity, characterized by the decline of dendritic spines, the expression of postsynaptic density 95 (PSD95), and synaptophysin (Syn) in the stressed Hipp along with the reduction of Wnt3a and beta-catenin, and increased GSK-3 beta. EA significantly alleviated PTSD-like behaviors, as assessed by the open field test, elevated platform maze test and conditioning fear test. This was paralleled by correcting abnormal neural plasticity by promoting the expression of PSD95 and Syn, as well as the number of dendritic spines in the Hipp. Importantly, EA exerted anti-PTSD effects by augmenting the expression levels of Wnt3a and beta-catenin, and decreasing that of GSK-3 beta. The effects mediated by EA were abolished by XAV939, an inhibitor of the Wnt/beta-catenin pathway. This suggests that EA relieved ESPS-induced PTSD-like behaviors, which can largely be ascribed to impaired neural plasticity in the Hipp. These findings provide new insights into possible mechanisms linking neural plasticity in the Hipp as potential novel targets for PTSD treatment in EA therapy.
引用
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页数:11
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