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在患有慢性炎症性疼痛相关抑郁症的老鼠中,电 ?? 疗法通过升调BDNF/TrkB/CREB信号通路来促进突触可塑性

Pu Yang¹, Haiyan Chen², Tian Wang¹

¹The First School of Clinical Medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi, China.

Brain and behavior

|November 10, 2023

概括

电针 (EA) 通过增强海马突触可塑性来缓解慢性炎症性疼痛和抑郁症. 这种疗法激活了BDNF/TrKB/CREB通路,为治疗与疼痛相关的情绪障碍提供了一个新的机制.

科学领域:

神经科学是一个神经科学.
疼痛研究疼痛研究
综合医学是一个整体的医学.

背景情况:

慢性炎症性疼痛 (CIP) 通常与抑郁症同时发生.
改变的神经突触可塑性与疼痛和抑郁症的发展有关.
已知电 ?? 可以缓解CIP和抑郁症,但其机制需要进一步阐明.

研究的目的:

研究EA是否可以通过调节海马突触可塑性来缓解CIP和抑郁症.
为EA在治疗CIP相关抑郁症 (CIPD) 的有效性提供证据.

主要方法:

疼痛和抑郁的行为被评估在老鼠使用已建立的行为测试.
使用尼斯尔染色和传输电子显微镜检查海马神经元形态和超结构.
参与突触可塑性和神经传递的关键蛋白质和mRNA (例如PSD-95,BDNF,TrKB,CREB,5-HT,GABA,Glu) 通过西区块,qRT-PCR和ELISA进行了量化.

主要成果:

在CIPD大鼠中,EA治疗显著改善了疼痛过敏和抑郁行为.
EA保护海马神经元免受结构损伤,并使神经递质水平正常 (5-HT,GABA,Glu).
通过激活BDNF/TrKB/CREB信号通路,EA提高了突触相关蛋白质 (PSD-95,Syn) 的调节.

结论:

在CIPD的老鼠模型中,EA在改善疼痛和抑郁行为方面表现出有效性.
在CIPD中EA的治疗机制与通过BDNF/TrKB/CREB信号通路调节海马突触可塑性有关.

关键词:

在BDNF/TrKB/CREB信号通路中.慢性炎症性疼痛是一种慢性炎症性疼痛.抑郁抑郁症抑郁症抑郁症是一种电针是一种电针疗法.在海马体内,海马体突触性可塑性突触性可塑性

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