| Project/Area Number |
24592364
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Kobe Gakuin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TOKUYAMA Shogo 神戸学院大学, 薬学部 臨床薬学研究室 (70225358)
KASUYA Fumiyo 神戸学院大学, 薬学部 臨床薬学研究室 (80131522)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | GPR40/FFA1 / 疼痛 / オピオイド / 下行性疼痛制御機構 / GPR40 / 下行性疼痛抑制系 / 抗侵害作用 / 遊離脂肪酸 / 侵害 |
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| Outline of Final Research Achievements |
Previously, we have demonstrated that docosahexaenoic acid-induced antinociception may be mediated by the G protein-coupled receptor40/free fatty acid receptor 1 (GPR40/FFA1). Here, we examined the involvement of supraspinal GPR40/FFA1 signaling in the regulation of inhibitory pain control systems consisting of serotonergic and noradrenergic neurons. We demonstrated that GPR40/FFA1 was expressed by proopiomeranocortin, serotonergic and noradrenergic neurons. In addition, these descending neurons were directly or indirectly activated by the administration of a GPR40/FFA1 agonist. Furthermore, GPR40/FFA1 agonist suppresses inflammatory pain, whereas it’s antagonism exacerbated formalin-induced pain, suggesting that the supraspinal GPR40/FFA1 signaling plays an important role in the regulation of the descending pain control system. Our findings provide insight into the mechanisms underlying intractable pain and may help in the development of therapeutic strategies for this ailment.
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