2013 Fiscal Year Final Research Report
Inhibitory modulation of the pain sensor protein, TRPA1
Project/Area Number |
23590730
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pain science
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Research Institution | Hyogo University of Health Sciences |
Principal Investigator |
DAI YI 兵庫医療大学, 薬学部, 准教授 (20330441)
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Project Period (FY) |
2011 – 2013
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Keywords | TRPA1 / TRPV1 / artemin / resveratrol / etodolac |
Research Abstract |
The transient receptor potential (TRP) channel subtype V1 (TRPV1) and A1 (TRPA1) are known to be expressed on sensory neurons and respond to changes in temperature, pH and local application of certain noxious chemicals. In this study, we investigated mechanisms of inhibitory modulation of these TRP channels. Following is the major findings of this study. 1. We found that artemin or resveratrol can inhibit TRPA1. The mechanism is likely due to a decreasing of the channel density of TRPA1 on cell membranes. 2. Pinosylvin methyl ether can inhibit TRPV1 by changing the EC50, but not the maximum response of capsaicin-induced currents. 3. Etodolac can direct activate and subsequently desensitize TRPA1 through a covalent modification of cysteine residues. These data indicate that the inhibitory mechanism of modulation of TRP channels are various and complicated.
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Research Products
(21 results)
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[Journal Article] Potentiation of the P2X3 ATP receptor by PAR-2 in rat DRG neurons, through protein kinase-dependent mechanisms, contributes to inflammatory pain2012
Author(s)
Wang S, Dai Y, Kobayashi K, Zhu W, Kogure Y, Yamanaka H, Wan Y, Zhang W, Noguchi K
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Journal Title
Eur J Neurosci
Volume: 36(3)
Pages: 2293-301
DOI
Peer Reviewed
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