p38 phosphorylation in medullary microglia mediates ectopic orofacial inflammatory pain in rats

Masaaki Kiyomoto, Masamichi Shinoda, Kuniya Honda, Yuka Nakaya, Ko Dezawa, Ayano Katagiri, Satoshi Kamakura, Tomio Inoue, Koichi Iwata

研究成果: ジャーナルへの寄稿記事査読

22 被引用数 (Scopus)

抄録

Background: Orofacial inflammatory pain is likely to accompany referred pain in uninflamed orofacial structures. The ectopic pain precludes precise diagnosis and makes treatment problematic, because the underlying mechanism is not well understood. Using the established ectopic orofacial pain model induced by complete Freund's adjuvant (CFA) injection into trapezius muscle, we analyzed the possible role of p38 phosphorylation in activated microglia in ectopic orofacial pain. Results: 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). Intra-cisterna successive administration of a p38 mitogen-activated protein kinase selective inhibitor, SB203580, suppressed microglial activation and its phosphorylation of p38. Moreover, SB203580 administration completely suppressed mechanical allodynia in the lateral facial skin and enhanced WDR neuronal excitability in Vc. Microglial interleukin-1β over-expression in Vc was induced by trapezius muscle inflammation, which was significantly suppressed by SB203580 administration. Conclusions: 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.

本文言語英語
論文番号48
ジャーナルMolecular Pain
11
1
DOI
出版ステータス出版済み - 12 8月 2015

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