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CCL2通过NMDA信号传递在前扣状皮层中增强了炎症疼痛和相关的焦虑行为

Huan Guo^1,2, Wen-Chao Hu², Hang Xian³

¹Department of Basic Medical Sciences, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, China.

Molecular neurobiology

|December 29, 2023

概括

在前带皮质 (ACC) 中的C-C动机化学因配体2 (CCL2) 途径驱动炎症性疼痛和焦虑. 阻止ACC中的CCR2受体通过调节N-甲基-D-酸盐受体 (NMDARs) 来减少这些症状.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
药理学药理学是一个学科.

背景情况:

C-C 基因化学因子连接体2 (CCL2) 与慢性疼痛和焦虑有关,但其在神经系统中的确切机制尚不清楚.
炎症性疼痛和类似焦虑的行为是严重的健康问题,需要对潜在的分子通路进行研究.

研究的目的:

研究前带带皮质 (ACC) 中CCL2-CCR2信号传导在完全弗洛恩德辅助剂 (CFA) 诱导的炎症性疼痛和焦虑类行为中的作用.
探索谷氨酸性N-甲基-D-酸盐受体 (NMDARs) 在这种途径中的参与.

主要方法:

在动物模型中,植入内注射CFA诱导炎症性疼痛和焦虑类行为.
局部双边注射CR2抗剂和NMDAR亚单元 (NR2B) 抑制剂到ACC.
评估疼痛和类似焦虑的行为.
在ACC中测量CCR2和CCL2表达.
全细胞补丁记录以分析突触电流 (mEPSC) 和NMDAR诱导的电流.

主要成果:

植入式CFA注射显著增加了ACC中的CCL2和CCR2表达,CCR2主要在刺激神经元上发现.
在ACC中局部使用CCR2抗剂减轻了CFA诱导的炎症性疼痛和焦虑类行为.
在ACC神经元中,CCR2抑制降低了微型刺激后突触电流 (mEPSC) 的频率.
在病理条件下,发现CCL2可以调节NMDAR诱导的神经元中ACC神经元的电流.
抑制NMDARs的NR2B亚单元减弱了CCL2诱导的过敏症和类似焦虑的行为.

结论:

CCL2通过CCR2作用于ACC刺激神经元,以调节CFA诱导的炎症性疼痛和相关的焦虑类行为,部分是通过NR2B子单元的上调调节.
在ACC中的CCL2-CCR2信号通路,特别是涉及NMDARs,代表了慢性炎症性疼痛和相关焦虑障碍的潜在治疗标.

关键词:

前环状皮层 (ACC) 的前环状皮层 (ACC) 的前环状皮层.慢性疼痛是一种慢性疼痛.这种NMDA受体是NMDA受体.在CC基因化基因连接体2 (CCL2) 中.在CC基因化基因受体2 (CCR2) 中.

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