Elucidation of the various mechanism of the pain mediated by GPR34

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K24067
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0907:Oral science and related fields
• Research Institution: Nagoya University
• Principal Investigator: Sayo Akira 名古屋大学, 医学部附属病院, 医員 (50849445)
• Project Period (FY): 2019-08-30 – 2022-03-31
• Keywords: 神経障害性疼痛 / GPR34 / ミクログリア / マクロファージ / 肥満細胞

Outline of Final Research Achievements

The signaling pathways of GPR34 for neuropathic pain other than microglia were evaluated behaviorally and histologically in mice. Intrathecal administration of LysoPS, a ligand for GPR34, slightly reduced pain in both mast cell-deficient and macrophage-deficient mice. Histological evaluation of LysoPS before and after intrathecal administration showed that mast cells had different degrees of degranulation but were not significant. No clear difference was confirmed for macrophages before and after administration. GPR34-mediated pain may involve cells focused on this study, and it is suggested that more detailed analysis of these pain mechanisms may advance the elucidation of neuropathic pain.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

神経障害性疼痛は持続的な病的疼痛であり、多くは慢性的な経過をたどる。この難治性疼痛の発症メカニズムは不明の点が多く、その解明により新たな治療法の開発が求められている。本研究は神経障害性疼痛の悪化に関与するGPR34のミクログリア以外の関与の可能性を示した。本研究が今後の治療法の開発や難治性の神経障害性疼痛の発生メカニズムの解明の一助になることが期待される。