电针减轻单次长时间应激小鼠的焦虑并调节杏仁核CRH/CRHR1信号。

Jing Zhu, Chang Wang, Yu Wang, Chunxia Guo, Pingping Lu, Fangfang Mou, Shuijin Shao
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引用次数: 4

摘要

背景:创伤后应激障碍(PTSD)是一种与焦虑相关的精神障碍,具有较高的焦虑症合并症。其潜在的神经生物学机制与下丘脑-垂体-肾上腺(HPA)轴功能障碍和应激激素有关。促肾上腺皮质激素释放激素(CRH)是一种主要的应激激素,在下丘脑和杏仁核中表达。电针(EA)可以改善情绪障碍,但其机制尚未完全阐明。本研究旨在观察EA对PTSD的治疗作用,并探讨其作用机制。方法:采用单只延长应激(SPS)小鼠建立创伤后应激障碍模型,在SPS后或7 d后进行EA治疗,持续一周。然后通过线索诱导恐惧条件测试、开放场测试和高架零迷宫观察小鼠的恐惧和焦虑样行为。测定EA干预后SPS小鼠杏仁核中CRH和CRH受体1 (CRHR1)蛋白水平。结果:我们发现在ST36和GV20处EA改善了SPS小鼠的恐惧和焦虑行为。SPS小鼠的杏仁核CRH和CRHR1蛋白水平升高,EA干预逆转了这种影响。CRHR1拮抗剂NBI 27914抑制CRHR1可减轻SPS小鼠的焦虑行为。结论:杏仁核中CRH/CRHR1信号通路可能参与EA对SPS小鼠的抗焦虑作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroacupuncture alleviates anxiety and modulates amygdala CRH/CRHR1 signaling in single prolonged stress mice.

Background: Post-traumatic stress disorder (PTSD) is an anxiety-related psychiatric disorder, manifesting high comorbidity with anxiety disorders. Its underlying neurobiological mechanisms have been associated with hypothalamic-pituitary-adrenal (HPA) axis dysfunction and stress hormones. Corticotropin-releasing hormone (CRH) is a primary stress hormone, expressed in the hypothalamus and amygdala. Electroacupuncture (EA) can improve mood disorders, but its mechanisms have not been fully elucidated. The aim of this study was to observe the effect of EA on PTSD and explore the related mechanisms.

Methods: We used single prolonged stress (SPS) mice to establish a PTSD model, and EA was performed after SPS or 7 days later for a week. Then we observed their fear and anxiety-like behavior through cue-induced fear condition tests, open field test and the elevated zero maze. CRH and CRH receptor 1 (CRHR1) protein levels in the amygdala were measured in SPS mice after EA intervention.

Results: We found that EA at ST36 and GV20 improved fear and anxiety behavior in SPS mice. The amygdala CRH and CRHR1 protein levels increased in the SPS mice, and this effect was reversed by the EA intervention. CRHR1 inhibition by the CRHR1 antagonist NBI 27914 alleviated anxiety behavior in SPS mice.

Conclusion: CRH/CRHR1 signaling in the amygdala may contribute to the anxiolytic effect of EA in SPS mice.

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