Involvement of ion channels in muscle hyperalgesia, intermittent claudication and cold allodynia in a new rat model of peripheral arterial disease.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24790575
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pain science
• Research Institution: Kanazawa University
• Principal Investigator: HORI Kiyomi 金沢大学, 医学系, 助教 (40595443)
• Research Collaborator: OZAKI Noriyuki 金沢大学, 医学系, 教授 ; YAMAGUCHI Takeshi 金沢大学, 医学系, 助教 ; SHIRAISHI Yoshitake 金沢大学, 医学系, 技術専門職員 ; NAKAMURA Tsuneo 金沢大学, 医学系, 技術専門職員
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 末梢動脈疾患 / PAD / 虚血性疼痛 / 筋痛 / 間歇性跛行 / 冷痛覚過敏 / ASIC3 / P2X3

Outline of Final Research Achievements

Aim: To demonstrate neuronal mechanisms underlying pain associated with peripheral arterial disease (PAD), we investigated the role of ion channels in a newly developed rat model of PAD. Methods: We ligated the rat’s left common iliac and iliolumbar arteries completely. Then, we assessed mechanical, thermal, cold sensitivity and intermittent claudication on behavioral testing. We also evaluated effects of antagonists to TRPV1, P2X3,2/3 ASICs, TRPA1 and TRPM8 on behavioral responses. Result: Chronic mechanical hyperalgesia of the muscle, reduced walking distance intermittent claudication and cold allodynia was observed after ligation. Antagonists against P2X3,2/3 and ASICs suppressed both muscle hyperalgesia and intermittent claudication and antagonists against TRPA1 suppressed cold allodynia in PAD rats. Conclusions: P2X3,2/3,ASICs and TRPA1 may play important roles in this model, and thus may be promising therapeutic targets for chronic ischemia-induced pain associated with PAD.

Free Research Field

神経科学