mGluR5 regulates inflammatory pain and pain aversion of CFA mice by mediating ERK/PI3K signaling pathway

IF 2 4区医学 Q3 NEUROSCIENCES

Neuroscience Letters Pub Date : 2025-05-29 DOI:10.1016/j.neulet.2025.138281

Zhuang Tianxin , Huang Zhongyu , Zhang Weishan , Wang Can , Lin Jiahong , Wang Shuhan , Zhang Runheng , Zhou Chang , Ma Yuxin

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引用次数: 0

Abstract

To investigate whether metabotropic glutamate receptor 5 (mGluR5) in the basolateral amygdala (BLA) regulates inflammatory pain and pain aversion by mediating ERK/PI3K signaling pathway in mice. Two experimental routes were designed. In route 1, 18 male C57BL/6 mice were divided into control, IFA, and CFA groups. In route 2, 18 mice received stereotaxic BLA injections of ACSF, the mGluR5 agonist DHPG, or antagonist MTEP on day 8 following CFA administration. Pain behaviors and aversive emotions were assessed over 14 days. BLA tissues were collected on day 15 for immunofluorescence staining and Western blot analyses of mGluR5, PI3K, p-PI3K, and ERK1/2 expression. The expression levels of p-PI3K, mGluR5 and ERK1/2 in the BLA of CFA mice were significantly increased, suggesting that their activation was associated with inflammatory pain. DHPG increased the expression of p-PI3K and mGluR5 and ERK1/2 in the CFA mouse brain BLA, while MTEP had the opposite effect. Our results show that mGluR5 regulates inflammatory pain and pain aversion of CFA mice by mediating the ERK/PI3K signaling pathway.

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mGluR5通过介导ERK/PI3K信号通路调节CFA小鼠炎症性疼痛和疼痛厌恶。

探讨杏仁核基底外侧（BLA）代谢性谷氨酸受体5 （mGluR5）是否通过介导ERK/PI3K信号通路调节小鼠炎症性疼痛和疼痛厌恶。设计了两条实验路线。途径1将18只雄性C57BL/6小鼠分为对照组、IFA组和CFA组。在途径2中，18只小鼠在给药后第8天接受立体定向BLA注射ACSF、mGluR5激动剂DHPG或拮抗剂MTEP。在14 天内评估疼痛行为和厌恶情绪。第15天收集BLA组织进行免疫荧光染色和Western blot分析mGluR5、PI3K、p-PI3K和ERK1/2的表达。p-PI3K、mGluR5和ERK1/2在CFA小鼠BLA中的表达水平显著升高，提示其激活与炎症性疼痛有关。DHPG增加了CFA小鼠脑BLA中p-PI3K、mGluR5和ERK1/2的表达，而MTEP的作用相反。我们的研究结果表明，mGluR5通过介导ERK/PI3K信号通路调节CFA小鼠的炎症性疼痛和疼痛厌恶。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroscience Letters 医学-神经科学

CiteScore

5.20

自引率

0.00%

发文量

408

审稿时长

50 days

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