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Microglia in the Primary Somatosensory Barrel Cortex Mediate
hM4D(Gi)-mCherry and hM3D(Gq)-mCherry were used for chemogenetics manipulation to inhibit or excite of the GluS1BF neuronal activity. (All viruses were packaged by BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Chemogenetics  PT-0043 rAAV-Ef1α-DIO-hM4D(Gi)-mCherry-WPRE-pA
 PT-0042 rAAV-Ef1α-DIO-hM3D(Gq)-mCherry-WPRE-pA
Yuping Wang, Peng Cao, Lisheng Mei, Weiwei Yin, Yu Mao, Chaoshi Niu, Zhi Zhang, and Wenjuan Tao
Pub Date: 2019-08-21,  DOI: 10.1016/j.neuroscience.2019.05.034, Email:
Abstract—Trigeminal 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.
Fig. 1 Activation of microgliaS1BF after CCI-ION.
In this study, using a model of TGN in mice with chronic constriction injury of the infraorbital nerve (CCI-ION), the authors identified changes in the activity of GluS1BF and microgliaS1BF cells, and their roles in the development of TGN. Furthermore, combining microglial cell morphological reconstruction, chemogenetic (From BrainVTA), electrophysiological and pharmacological methods, they described the putative importance of microglia as a key regulator in TGN through actions on GluS1BF neuronal adaptation.
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