Electroacupuncture Ameliorates Depression-Like Behaviour in Rats by Enhancing Synaptic Plasticity via the GluN2B/CaMKII/CREB Signalling Pathway

Kun Zhang; Ran Liu; Jingruo Zhang; Xifang Wei; Yuan Gao; Wen Ma; Yijing Li; Wa Cai; Weidong Shen

doi:10.1155/2021/2146001

Electroacupuncture Ameliorates Depression-Like Behaviour in Rats by Enhancing Synaptic Plasticity via the GluN2B/CaMKII/CREB Signalling Pathway

Evid Based Complement Alternat Med. 2021 Nov 3:2021:2146001. doi: 10.1155/2021/2146001. eCollection 2021.

Authors

Kun Zhang^{1

2}, Ran Liu^{1

2}, Jingruo Zhang^{1

2}, Xifang Wei^{1

2}, Yuan Gao¹, Wen Ma¹, Yijing Li¹, Wa Cai^{1

2}, Weidong Shen^{1

2}

Affiliations

¹ Department of Acupuncture, Shuguang Hospital affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
² Institute of Acupuncture and Anesthesia, Shuguang Hospital affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.