The role of mechanically-sensitive ion channels in delayed onset muscle soreness

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K11246
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 59010:Rehabilitation science-related
• Research Institution: Niigata University of Health and Welfare
• Principal Investigator: Ota Hiroki 新潟医療福祉大学, リハビリテーション学部, 助教 (10712432)
• Co-Investigator(Kenkyū-buntansha): 片野坂 友紀 岡山大学, 医歯薬学総合研究科, 講師 (60432639)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 痛み / 侵害受容器 / 機械受容チャネル

Outline of Final Research Achievements

Delayed onset muscle soreness (DOMS) is mechanical hyperalgesia that occurs after uncustomed exercise, but the involvement of mechanosensitive ion channels in the soreness remains unknown. In this study, we carried out experiments using behavioral and biochemical techniques to identify the mechanosensitive ion channels that involved in the onset of the soreness. We found that TRPA1, not TRPV2, is involved in muscle mechanical hyperalgesia in DOMS. Furthermore, the expression level of Tmem120A, a novel mechanoreceptor candidate, was increased, compatible with that of mechanical hyperalgesia behavior. Gene expression analysis on rat RNA-seq data suggests that Dusp-15 can be a new candidate for involvement in generating of DOMS.

Free Research Field

環境生理学（含体力医学・栄養生理学）

Academic Significance and Societal Importance of the Research Achievements

肩こりや腰痛をはじめとする筋・筋膜性疼痛症候群は骨格筋に起因する痛みであり、罹患者数がきわめて多い。それにもかかわらず、他の組織に起因する痛みに比べ不明な点が多く、その根本的治療法の開発が急がれる。「遅発性筋痛モデル」は筋・筋膜性疼痛症候群を再現したモデルと考えられており、今回、当モデルにおいて新たな本症候発症因子が複数同定された。これらの成果は、骨格筋の痛み機構の学術的意義を有するとともに、骨格筋の痛み治療における全く新しい創薬分野の発展に寄与することが期待される。