p38 phosphorylation and caspase1 in medullary microglia mediates ectopic orofacial inflammatory

2014 Fiscal Year Final Research Report

• Project/Area Number: 25893261
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Functional basic dentistry
• Research Institution: Showa University (2014); Nihon University (2013)
• Principal Investigator: HAN In Yang 昭和大学, 歯学部, 助教 (00712556)
• Research Collaborator: INOUE Tomio 昭和大学, 歯学部口腔生理学講座, 教授 (70184760) ; IWATA Kouichi 日本大学, 歯学部口腔生理学講座, 教授 (60160115) ; SHINODA Masamichi 日本大学, 歯学部口腔生理学講座, 准教授 (20362238) ; NAKAMURA Shiro 昭和大学, 歯学部口腔生理学講座, 講師 (60384187) ; MOCHIZUKI Ayako 昭和大学, 歯学部口腔生理学講座, 助教 (10453648) ; NAKAYAMA Kiyomi 昭和大学, 歯学部口腔生理学講座, 助教 (00433798)
• Project Period (FY): 2013-08-30 – 2015-03-31
• Keywords: microglia / p38MAPK / IL-1β / 顎顔面部異常疼痛 / 異所性異常疼痛 / 疼痛 / 関連痛 / 神経生理学

Outline of Final Research Achievements

Mechanical allodynia in the lateral facial skin was induced following trapezius muscle inflammation, which accompanied microglial activation with p38 phosphorylation and hyperexcitability of wide dynamic range (WDR) neurons in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2). p38 mitogen-activated protein kinase selective inhibitor administration completely suppressed mechanical allodynia in the lateral facial skin and activation of microglia, Interleukin-1β. Moreover, WDR neuronal excitability in Vc and C1-C2 was significantly suppressed by inhibitor These findings indicate that microglia, activated via p38 phosphorylation, play a pivotal role in WDR neuronal hyperexcitability, which accounts for the mechanical hypersensitivity in the lateral facial skin associated with trapezius muscle inflammation. I submitted these date a paper to Molecular Pain (2015.5.22).

Free Research Field

生理学