2. Academic Validation
  3. Microglia in the Primary Somatosensory Barrel Cortex Mediate Trigeminal Neuropathic Pain

Microglia in the Primary Somatosensory Barrel Cortex Mediate Trigeminal Neuropathic Pain

  • Neuroscience. 2019 Aug 21;414:299-310. doi: 10.1016/j.neuroscience.2019.05.034.
Yuping Wang 1,  Peng Cao 1,  Lisheng Mei 1,  Weiwei Yin 1,  Yu Mao 2,  Chaoshi Niu 3,  Zhi Zhang 4,  Wenjuan Tao 5
Affiliations

Affiliations

  • 1 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.
  • 2 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; Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230022, PR China.
  • 3 Department of Neurosurgery, The First Affiliated Hospital of University of Science and Technology of China, Hefei 230001, PR China.
  • 4 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. Electronic address: [email protected].
  • 5 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; Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230022, PR China. Electronic address: [email protected].
PMID: 31181369 DOI: 10.1016/j.neuroscience.2019.05.034
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.

Keywords

Chronic constriction injury; glutamatergic neurons; microglia; trigeminal neuropathic pain.

Figures
Products