| Literature DB >> 33067780 |
Qian Li1, Tian-Le Ma1, You-Qi Qiu1, Wen-Qiang Cui1,2, Teng Chen1, Wen-Wen Zhang1, Jing Wang3, Qi-Liang Mao-Ying1, Wen-Li Mi1, Yan-Qing Wang1, Yu-Xia Chu4.
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.Entities:
Keywords: Gap junction; Glutamate receptor ionotropic kainate 2; Orofacial pain; Transient receptor potential A1
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Year: 2020 PMID: 33067780 PMCID: PMC7719140 DOI: 10.1007/s12264-020-00594-4
Source DB: PubMed Journal: Neurosci Bull ISSN: 1995-8218 Impact factor: 5.203