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电针对海马神经元的生存和突触可塑性以及改善睡眠剥夺引起的空间记忆损伤具有促进作用。

Electroacupuncture promotes the survival and synaptic plasticity of hippocampal neurons and improvement of sleep deprivation-induced spatial memory impairment.

机构信息

Department of Acupuncture, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Department of Histology and Embryology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.

出版信息

CNS Neurosci Ther. 2021 Dec;27(12):1472-1482. doi: 10.1111/cns.13722. Epub 2021 Oct 8.

DOI:10.1111/cns.13722
PMID:34623740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8611786/
Abstract

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.

摘要

目的

本研究旨在探讨电针对空间记忆损伤大鼠的治疗作用及其可能的机制,即电针是否通过激活脑源性神经营养因子(BDNF)/酪氨酸受体激酶(TrkB)/细胞外信号调节激酶(Erk)信号通路促进海马神经元的存活和突触可塑性,从而改善其空间记忆缺陷。

方法

在体内,通过 Morris 水迷宫(MWM)检测电针对学习记忆的影响,同时采用 Western blot(WB)、免疫荧光(IF)和透射电镜(TEM)技术探讨海马神经元和突触的可塑性以及 BDNF/TrkB/Erk 信号通路的表达。在体外,用外源性 BDNF 和 TrkB 抑制剂 K252a 处理培养的海马神经元,以确认 BDNF/TrkB/Erk 信号通路与突触可塑性之间的关系。

结果

我们的结果表明,电针减轻了空间记忆损伤大鼠海马神经元和突触的丢失,刺激了海马神经发生,并改善了其学习和记忆能力,同时伴随着 BDNF 的上调和 TrkB 及 Erk 的磷酸化增加。在培养的海马神经元中,外源性 BDNF 增强了突触蛋白的表达、突触后电流的频率以及 TrkB 和 Erk 的磷酸化;这些作用可被 K252a 逆转。

结论

电针通过激活 BDNF/TrkB/Erk 信号通路促进海马神经元的发生和突触可塑性,从而减轻空间记忆损伤大鼠的空间记忆损伤,为电针对认知障碍的治疗作用提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/c1b712803bff/CNS-27-1472-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/3d9209821a6a/CNS-27-1472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/4753cf1c60a0/CNS-27-1472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/64b8ce0612c9/CNS-27-1472-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/1144b432c929/CNS-27-1472-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/9e978203dbc2/CNS-27-1472-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/c1b712803bff/CNS-27-1472-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/3d9209821a6a/CNS-27-1472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/4753cf1c60a0/CNS-27-1472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/64b8ce0612c9/CNS-27-1472-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/1144b432c929/CNS-27-1472-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/9e978203dbc2/CNS-27-1472-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/8611786/c1b712803bff/CNS-27-1472-g006.jpg

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