Open AccessElectroacupuncture promotes the survival and synaptic plasticity of hippocampal neurons and improvement of sleep deprivation‐induced spatial memory impairment
Author(s) -
Pei Wenya,
Meng Fanqi,
Deng Qingwen,
Zhang Baobao,
Gu Yuan,
Jiao Boyu,
Xu Haoyu,
Tan Jiuqing,
Zhou Xin,
Li Zhiling,
He Guanheng,
Ruan Jingwen,
Ding Ying
Publication year - 2021
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.13722
Subject(s) - tropomyosin receptor kinase b , hippocampal formation , neuroscience , synaptic plasticity , brain derived neurotrophic factor , neurotrophic factors , hippocampus , morris water navigation task , neurogenesis , mapk/erk pathway , long term potentiation , biology , medicine , microbiology and biotechnology , signal transduction , receptor
Aims This study aimed to investigate whether electroacupuncture (EA) promotes the survival and synaptic plasticity of hippocampal neurons by activating brain‐derived neurotrophic factor (BDNF)/tyrosine receptor kinase (TrkB)/extracellular signal‐regulated kinase (Erk) signaling, thereby improving spatial memory deficits in rats under SD. Methods In vivo, Morris water maze (MWM) was used to detect the effect of EA on learning and memory, at the same time Western blotting (WB), immunofluorescence (IF), and transmission electron microscopy (TEM) were used to explore the plasticity of hippocampal neurons and synapses, and the expression of BDNF/TrkB/Erk signaling. In vitro, cultured hippocampal neurons were treated with exogenous BDNF and the TrkB inhibitor K252a to confirm the relationship between BDNF/TrkB/Erk signaling and synaptic plasticity. Results Our results showed that EA mitigated the loss of hippocampal neurons and synapses, stimulated hippocampal neurogenesis, and improved learning and memory of rats under SD accompanied by upregulation of BDNF and increased phosphorylation of TrkB and Erk. In cultured hippocampal neurons, exogenous BDNF enhanced the expression of synaptic proteins, the frequency of the postsynaptic currents, and the phosphorylation of TrkB and Erk; these effects were reversed by treatment with K252a. Conclusions Electroacupuncture alleviates SD‐induced spatial memory impairment by promoting hippocampal neurogenesis and synaptic plasticity via activation of BDNF/TrkB/Erk signaling, which provided evidence for EA as a therapeutic strategy for countering the adverse effects of SD on cognition.