作者: Yuping Wang , Peng Cao , Lisheng Mei , Weiwei Yin , Yu Mao
DOI: 10.1016/J.NEUROSCIENCE.2019.05.034
关键词: Sensitization 、 Neuropathic pain 、 Glutamatergic 、 Electrophysiology 、 Barrel cortex 、 Medicine 、 Microglia 、 Premovement neuronal activity 、 Somatosensory system 、 Neuroscience
摘要: 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 primary somatosensory barrel cortex (S1BF), which a critical region for TGN, mouse model that displayed significant pain-related behaviors. Using electrophysiological recordings, found robust neuronal hyperactivity glutamatergic neurons S1BF (GluS1BF). Chemogenetic inhibition GluS1BF significantly relieved mechanical allodynia mice. naive mice, chemogenetic activation induced sensitization. addition, (microgliaS1BF) were activated, with density and morphology changes. Intraperitoneal administration minocycline, inhibitor, attenuated sensitization, decreased Together, these findings demonstrate putative importance as key regulator through actions on adaptation.