Jiang Li, Zhang Hao, Zhou Junhe, Tang Xiaorong, Luo Le, Huang Peidong, Yi Wei, Xu Nenggui, Liu Jianhua, Fu Wenbin
Department of Acupuncture and Moxibustion, The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong, China; Acupuncture Research Team, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Acupuncture Research Team, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
World Neurosurg. 2020 Jul;139:e455-e462. doi: 10.1016/j.wneu.2020.04.042. Epub 2020 Apr 18.
A large body of evidence has suggested that the disruptions of neural plasticity in the brain play a pivotal role in major depressive disorder (MDD). Electroacupuncture (EA) therapy has been shown to be an effective treatment modality for MDD. However, the mechanism underling the antidepressive effect of EA treatment has not been clearly elucidated. This study aimed to investigate the antidepressant-like effects of EA associated with its protection effect of synaptic structural plasticity.
An MDD model was induced by exposing Sprague Dawley rats to chronic unpredictable mild stress (CUMS). EA stimulation (Hegu and Taichong) and AMPA receptor (AMPAR) antagonist NBQX intrahippocampal injection were used to treat the depressed rats.
We found EA improved behavioral performance, enhanced synaptic structural plasticity, and upregulated gene and protein levels of GluR1, GluR2, Stargazin, Pick1, SYP, PSD-95, and GAP-43. AMPAR antagonist NBQX had the opposite effect on behavioral performance, synaptic plasticity, and the aforementioned genes and proteins.
These results suggest that EA has a potent antidepressant effect, likely through upregulated expression of the AMPAR and protected neural plasticity in CUMS-treated rats.
大量证据表明,大脑中神经可塑性的破坏在重度抑郁症(MDD)中起关键作用。电针(EA)疗法已被证明是治疗MDD的有效方法。然而,EA治疗抗抑郁作用的潜在机制尚未明确阐明。本研究旨在探讨EA的抗抑郁样作用及其对突触结构可塑性的保护作用。
通过将Sprague Dawley大鼠暴露于慢性不可预测轻度应激(CUMS)来诱导MDD模型。采用EA刺激(合谷和太冲)和海马内注射AMPA受体(AMPAR)拮抗剂NBQX来治疗抑郁大鼠。
我们发现EA改善了行为表现,增强了突触结构可塑性,并上调了GluR1、GluR2、Stargazin、Pick1、SYP、PSD - 95和GAP - 43的基因和蛋白水平。AMPAR拮抗剂NBQX对行为表现、突触可塑性以及上述基因和蛋白具有相反的作用。
这些结果表明,EA具有强大的抗抑郁作用,可能是通过上调CUMS处理大鼠中AMPAR的表达并保护神经可塑性来实现的。