Jiang Shuo, Shen Zui, Xu Wenlin
The First Affiliated Hospital of Zhejiang University of Traditional Chinese Medicine, Hangzhou 310006, China.
Zhejiang University of Traditional Chinese Medicine, Hangzhou 310053, China.
Evid Based Complement Alternat Med. 2021 Nov 12;2021:9639131. doi: 10.1155/2021/9639131. eCollection 2021.
Depression is a global mental health problem with high disability rate, which brings a huge disease burden to the world. Electroacupuncture (EA) has been shown to be an effective method for the treatment of depression. However, the mechanism underling the antidepressant effect of EA has not been clearly clarified. The change of synaptic plasticity is the focus in the study of antidepressant mechanism. This study will observe the effect of EA on LTP of hippocampal synaptic plasticity and explore its possible mechanism.
The depression-like behavior rat model was established by chronic unpredictable mild stress (CUMS). EA stimulation (Hegu and Taichong) was used to treat the depressed rats. The depression-like behavior of rats was tested by weight measurement, open field test, depression preference test, and novelty suppressed feeding test. Long-term potentiation (LTP) was recorded at CA1 synapses in hippocampal slices by electrophysiological method. N-methyl-D-aspartate receptor subunit 2B (NR2B) and calmodulin-dependent protein kinase II (CaMK II) protein levels were examined by using western blot.
After the establishment of CUMS-induced depression model, the weight gain rate, sucrose preference rate, line crossing number, and rearing times of rats decreased, and feeding time increased. At the same time, the LTP in hippocampus was impaired, and the expressions of NR2B and CaMK II were upregulated. After EA treatment, the depression-like behavior of rats was improved, the impairment of LTP was reversed, and the expression levels of NR2B and CaMK II protein were downregulated.
EA can ameliorate depression-like behaviors by restoring LTP induction, downregulating NR2B and CaMK II expression in CUMS model rats, which might be part of the mechanism of EA antidepressant.
抑郁症是一种全球范围内致残率高的心理健康问题,给世界带来了巨大的疾病负担。电针已被证明是治疗抑郁症的有效方法。然而,电针抗抑郁作用的潜在机制尚未明确阐明。突触可塑性的变化是抗抑郁机制研究的重点。本研究将观察电针对海马突触可塑性长时程增强(LTP)的影响,并探讨其可能机制。
采用慢性不可预测性温和应激(CUMS)建立抑郁症样行为大鼠模型。用电针刺激(合谷和太冲)治疗抑郁大鼠。通过体重测量、旷场试验、抑郁偏好试验和新奇性抑制摄食试验检测大鼠的抑郁样行为。采用电生理方法记录海马脑片CA1突触处的长时程增强(LTP)。用蛋白质免疫印迹法检测N-甲基-D-天冬氨酸受体亚基2B(NR2B)和钙调蛋白依赖性蛋白激酶II(CaMK II)的蛋白水平。
建立CUMS诱导的抑郁模型后,大鼠体重增加率、蔗糖偏好率、穿越格数和直立次数降低,摄食时间增加。同时,海马LTP受损,NR2B和CaMK II表达上调。电针治疗后,大鼠的抑郁样行为得到改善,LTP损伤得到逆转,NR2B和CaMK II蛋白表达水平下调。
电针可通过恢复LTP诱导、下调CUMS模型大鼠NR2B和CaMK II表达来改善抑郁样行为,这可能是电针抗抑郁机制的一部分。