• Yuping Wang, Peng Cao, Lisheng Mei, Weiwei Yin, Yu Mao, Chaoshi Niu, Zhi Zhang, and Wenjuan Tao.
• Hefei National Laboratory for Physical Sciences at the Microscale, Key Laboratory of Brain Function and Disease, Department of Biophysics and Neurobiology, University of Science and Technology of China, Hefei 230027, PR China.
• Neuroscience. 2019 Aug 21; 414: 299-310.

AbstractTrigeminal neuropathic pain (TGN) is an attacking, abrupt, electric-shock headache involving abnormal cortical activity. The neural mechanism underlying TGN remains elusive. In this study, we explored the role of microglia in the primary somatosensory barrel cortex (S1BF), which is a critical region for TGN, of a mouse model of TGN that displayed significant pain-related behaviors. Using electrophysiological recordings, we found robust neuronal hyperactivity in glutamatergic neurons of S1BF (GluS1BF). Chemogenetic inhibition of GluS1BF neurons significantly relieved mechanical allodynia in TGN mice. In naïve mice, chemogenetic activation of GluS1BF neurons induced pain sensitization. In addition, we found that microglia in the S1BF (microgliaS1BF) were significantly activated, with density and morphology changes. Intraperitoneal administration of minocycline, a microglia inhibitor, attenuated pain sensitization, and decreased GluS1BF neuronal activity. Together, these findings demonstrate the putative importance of microglia as a key regulator in TGN through actions on GluS1BF neuronal adaptation.Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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