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连接蛋白36通过GluK2和TRPA1介导口面部疼痛超敏反应。

Connexin 36 Mediates Orofacial Pain Hypersensitivity Through GluK2 and TRPA1.

作者信息

Li Qian, Ma Tian-Le, Qiu You-Qi, Cui Wen-Qiang, Chen Teng, Zhang Wen-Wen, Wang Jing, Mao-Ying Qi-Liang, Mi Wen-Li, Wang Yan-Qing, Chu Yu-Xia

机构信息

Department of Integrative Medicine and Neurobiology, Institutes of Integrative Medicine, School of Basic Medical Sciences, Institutes of Brain Science, Brain Science Collaborative Innovation Center, State Key Laboratory of Medical Neurobiology, and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, 200031, China.

Department of Pain Management, Shandong Provincial Qianfoshan Hospital, The First Hospital Affiliated with Shandong First Medical University, Jinan, 250000, China.

出版信息

Neurosci Bull. 2020 Dec;36(12):1484-1499. doi: 10.1007/s12264-020-00594-4. Epub 2020 Oct 16.

Abstract

Trigeminal neuralgia is a debilitating condition, and the pain easily spreads to other parts of the face. Here, we established a mouse model of partial transection of the infraorbital nerve (pT-ION) and found that the Connexin 36 (Cx36) inhibitor mefloquine caused greater alleviation of pT-ION-induced cold allodynia compared to the reduction of mechanical allodynia. Mefloquine reversed the pT-ION-induced upregulation of Cx36, glutamate receptor ionotropic kainate 2 (GluK2), transient receptor potential ankyrin 1 (TRPA1), and phosphorylated extracellular signal regulated kinase (p-ERK) in the trigeminal ganglion. Cold allodynia but not mechanical allodynia induced by pT-ION or by virus-mediated overexpression of Cx36 in the trigeminal ganglion was reversed by the GluK2 antagonist NS102, and knocking down Cx36 expression in Nav1.8-expressing nociceptors by injecting virus into the orofacial skin area of Nav1.8-Cre mice attenuated cold allodynia but not mechanical allodynia. In conclusion, we show that Cx36 contributes greatly to the development of orofacial pain hypersensitivity through GluK2, TRPA1, and p-ERK signaling.

摘要

三叉神经痛是一种使人衰弱的疾病,疼痛很容易扩散到面部的其他部位。在此,我们建立了眶下神经部分横断(pT-ION)的小鼠模型,发现与减轻机械性异常性疼痛相比,连接蛋白36(Cx36)抑制剂甲氟喹对pT-ION诱导的冷异常性疼痛有更大程度的缓解作用。甲氟喹逆转了pT-ION诱导的三叉神经节中Cx36、离子型红藻氨酸盐受体2(GluK2)、锚蛋白1型瞬时受体电位(TRPA1)和磷酸化细胞外信号调节激酶(p-ERK)的上调。GluK2拮抗剂NS102可逆转pT-ION或三叉神经节中病毒介导的Cx36过表达所诱导的冷异常性疼痛,但不能逆转机械性异常性疼痛,并且通过向Nav1.8-Cre小鼠的口面部皮肤区域注射病毒来敲低表达Nav1.8的伤害性感受器中的Cx36表达,可减轻冷异常性疼痛,但不能减轻机械性异常性疼痛。总之,我们表明Cx36通过GluK2、TRPA1和p-ERK信号通路对口面部疼痛超敏反应的发展有很大贡献。

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