Role of transient receptor potential melastatin 2 channels in visceral nociception and hypersensitivity in rats
| Project/Area Number |
25860395
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied pharmacology
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| Research Institution | Kyoto Pharmaceutical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 炎症性腸疾患 / 内臓痛 / 温度感受性受容体 / TRPM2 / 消化管炎症 / ヒト検体 |
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| Outline of Final Research Achievements |
TRPM2, which is a thermosensitive and Ca2+-permeable cation channel, contributes to the pathogenesis of inflammatory bowel disease. The present study investigated the expression of TRPM2 and their involvement in visceral sensitivity in rats. TRPM2 was expressed in enteric neuron, and was co-localized with the marker of intrinsic primary afferent neuron. The majority of TRPM cells were double positive with a retrograde marker fluorogold in DRG. TRPM2-positive DRG neurons were labeled with A-fiber, C-fiber marker, substance P, and CGRP. The TRPM2 inhibitor econazole reduced visceromotor response to noxious colorectal distention in the normal rats. The expression of TRPM2 in the mucosa was increased in TNBS-induced colitis models. Econazole attenuated the visceral hypersensitivity to the control level. In conclusion, TRPM2 expressed in intrinsic and spinal primary afferent neurons contributes to the visceral pain under normal and visceral hypersensitivity under inflammatory conditions.
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Report
(4 results)
Research Products
(18 results)
