These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Microglia in the Primary Somatosensory Barrel Cortex Mediate Trigeminal Neuropathic Pain.
    Author: Wang Y, Cao P, Mei L, Yin W, Mao Y, Niu C, Zhang Z, Tao W.
    Journal: Neuroscience; 2019 Aug 21; 414():299-310. PubMed ID: 31181369.
    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.
    [Abstract] [Full Text] [Related] [New Search]