| Project/Area Number |
26460713
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | Hyogo University of Health Sciences |
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Principal Investigator |
DAI YI 兵庫医療大学, 薬学部, 教授 (20330441)
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| Co-Investigator(Renkei-kenkyūsha) |
Yamamoto Satoshi 兵庫医療大学, 薬学部, 教授 (60220464)
Noguchi Koichi 兵庫医療大学, 医学部, 教授 (10212127)
Wang Shenglan 兵庫医療大学, 薬学部, 助教授 (50714359)
Kogure Yoko 兵庫医療大学, 薬学部, 助教授 (60548684)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | AMPK / TRPA1 / Pain |
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| Outline of Final Research Achievements |
AMP activated protein kinase (AMPK) is a widely expressed intracellular energy sensor that monitors and modulates energy expenditure. AMPK is activated in response to ATP consumption, and upon activation, AMPK phosphorylates a broad range of downstream targets, which results in a reduction in energy usage and an increase in energy production. Transient receptor potential ankyrin 1 (TRPA1) channel is a widely recognized chemical and thermal sensor that plays vital roles in pain transduction.
Here, we discovered a functional link between AMPK and TRPA1 in dorsal root ganglion (DRG) neurons, in which AMPK activation rapidly inhibit TRPA1 channel activity within minutes. These observation demonstrated an important role and the molecular mechanism of AMPK in pain generation.
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