Central sensitization is one of the important pathological mechanisms of chronic migraine (CM). Metabolic glutamate receptor 5 (mGluR5) mediates pain by activating various intracellular pathways. However, whether mGluR5 contributes to central sensitization in CM and the exact mechanism remains unclear. Male rats were used to establish a CM model by repeated infusions of inflammatory soup (IS) for 7 days to stimulate the activation of the dural nociceptor. The mechanical and thermal thresholds were used to evaluate allodynia, and central sensitization was assessed by measuring calcitonin gene-related peptide (CGRP) and substance P (SP). Microtubule associated protein 1 light chain 3 (LC3) and p62/SQSTM1 were used to assess autophagy. We found that the expression of mGluR5 in the trigeminal nucleus caudalis (TNC) of CM rats was significantly increased. In addition, the downregulation of mGluR5 activated autophagy by inhibiting the mTOR pathway. Moreover, the activation of autophagy alleviated allodynia and central sensitization in CM rats. This study identified a novel strategy for the treatment of CM; the downregulation of mGluR5 in a rat model of CM decreased the expression of the inflammatory factor interleukin-1 beta (IL-1β) and the central sensitization-associated proteins CGRP and SP by activating autophagy via inhibiting the mTOR pathway.

中枢敏化是慢性偏头痛（CM）的重要病理机制之一。代谢型谷氨酸受体5（mGluR5）通过激活各种细胞内途径来介导疼痛。但是，mGluR5是否有助于CM中枢敏化和确切的机制尚不清楚。通过反复输注炎性汤（IS）7天来刺激硬脑膜伤害感受器的活化，使用雄性大鼠建立CM模型。机械阈值和热阈值用于评估异常性疼痛，中枢敏化通过测量降钙素基因相关肽（CGRP）和P物质（SP）进行评估。微管相关蛋白1轻链3（LC3）和p62 / SQSTM1用于评估自噬。我们发现，CM大鼠三叉尾尾核（TNC）中mGluR5的表达显着增加。此外，mGluR5的下调通过抑制mTOR途径激活了自噬。此外，自噬的激活减轻了CM大鼠的异常性疼痛和中枢敏化。这项研究确定了一种新的治疗CM的策略。CM大鼠模型中mGluR5的下调通过抑制mTOR途径激活自噬，从而降低了炎症因子白介素1β（IL-1β）和中枢敏化相关蛋白CGRP和SP的表达。这项研究确定了一种新的治疗CM的策略。CM大鼠模型中mGluR5的下调通过抑制mTOR途径激活自噬，从而降低了炎症因子白介素1β（IL-1β）和中枢敏化相关蛋白CGRP和SP的表达。这项研究确定了一种新的治疗CM的策略。CM大鼠模型中mGluR5的下调通过抑制mTOR途径激活自噬，从而降低了炎症因子白介素1β（IL-1β）和中枢敏化相关蛋白CGRP和SP的表达。