Mechanisms of pain sensation through interactions between TRP channels and anoctamin 1

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19197
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pain science
• Research Institution: Okazaki Research Facilities, National Institutes of Natural Sciences
• Principal Investigator: TAKAYAMA Yasunori 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設), 岡崎統合バイオサイエンスセンター, 特任助教 (60711033)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: TRPV1 / アノクタミン1 / 疼痛

Outline of Final Research Achievements

TRPV1, a capsaicin receptor, is an important ion channel in sensory nerves to detect painful situation in skin. For long time, TRPV1 has been believed as main ion channel inducing burning pain, however we identified the interaction with anoctamin 1, a kind of chloride channel. This TRPV1-anoctamin 1 interaction is a molecular mechanism to enhance TRPV1-mediated pain sensation. In addition, capsaicin-induced pain was reduced by anoctamin 1 inhibitor. Thus, the painkiller targeting anoctamin 1 could be better therapy in clinical situations.
Furthermore, we found a new chemical compound which has inhibitory effect on anoctamin 1 activity. Therefore, this chemical could be novel seeds in the development of painkiller.

Free Research Field

神経生理学