Pathophysiological roles of TRP family members in a variety of neurological disorders

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390016
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Kyoto University
• Principal Investigator: KANEKO Shuji 京都大学, 薬学研究科(研究院), 教授 (60177516)
• Co-Investigator(Kenkyū-buntansha): NAKAGAWA Takayuki 京都大学, 大学院・医学研究科, 准教授 (30303845) ; SHIRAKAWA Hisashi 京都大学, 大学院・薬学研究科, 准教授 (50402798)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: TRPチャネル / グリア細胞 / 神経変性疾患 / 脳内炎症 / カチオン輸送

Outline of Final Research Achievements

To provide new insights into the molecular mechanisms and identify promising therapeutic targets are needed to elucidate the initiation and progression of neurological diseases. The importance of neurons, immune and glial cells in neurological diseases is becoming revealed and understood; however the pathophysiological roles of TRP channels in neurological diseases remain to be completely elucidated. In vitro and in vivo experiments demonstrate that 1) TRPC3 inhibitor Pyr3 improves outcomes after intracerebral hemorrhage in mice, 2) TRPC6 is involved in S1P-induced astrocytic responses, 3) TRPM2 contributes to LPS/ interferon gamma-induced production of nitric oxide in microglia, 4) Involvement of TRPA1 activation through oxidative modification oxaliplatin-induced acute peripheral neuropathy, 5) Activation of mitochondrial TRPV1 contributes to microglial migration, suggesting that the above-mentioned TRP channels may constitute a new therapeutic target for neurological disorders.

Free Research Field

薬理学