Elucidation of the mechanisms of chronic pain by PAC1 receptor and drug discovery.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430067
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurochemistry/Neuropharmacology
• Research Institution: University of Toyama
• Principal Investigator: TAKASAKI ICHIRO 富山大学, 大学院理工学研究部(工学), 准教授 (00397176)
• Co-Investigator(Renkei-kenkyūsha): KURIHARA TAKASHI 鹿児島大学, 医歯学総合研究科(医学), 准教授 (60282745) ; TOYOOKA NAOKI 富山大学, 大学院理工学研究部(工学), 教授 (10217565) ; GOUDA HIROAKI 昭和大学, 薬学部, 教授 (60276160)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: PACAP / PAC1受容体 / アロディニア / 脊髄後角 / マイクロアレイ / 創薬

Outline of Final Research Achievements

Activation of spinal PAC1 receptor induces long-lasting mechanical allodynia in mice. In this study, we analyzed the involvement spinal Cyr61 which expression is increased by PAC1 receptor activation on the pain. Intrathecal injection of Cyr61 recombinant protein induced mechanical allodynia. Cyr61 protein increased the expression of chemokine CCL2 and CCL7 mRNA via integrin beta-1 in the astrocyte. The present results suggest that spinal PAC1-Cyr61-chemokine signaling are involved in the chronic pain and that integrin and/or chemokine receptors may be useful target for developing new analgesics.

Free Research Field

神経薬理学，疼痛学