| Project/Area Number |
18K08836
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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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| Review Section |
Basic Section 55050:Anesthesiology-related
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| Research Institution | Kobe Gakuin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
徳山 尚吾 神戸学院大学, 薬学部, 教授 (70225358)
糟谷 史代 神戸学院大学, 薬学部, 教授 (80131522)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 疼痛 / 脂肪酸受容体 / 脂肪酸 / 視床下部 / 長鎖脂肪酸受容体 / GPR40 / ストレス |
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| Outline of Final Research Achievements |
In this study, brain phosphatidylcholines with docosahexaenoic acid, arachidonic acid and other long-chain fatty acids were found to have decreased in the brains of stressed mice with or without pain by using imaging mass spectrometry. Also, we demonstrated that some genes of fatty acid-related genes including iPLA2 and FABPs were changed in some brain areas of chronic pain model mice. So, endogenous agonist of a free fatty acid receptor GPR40/FFAR1 were decreased in stressed mice with or without pain. Therefore, we concluded that brain GPR40/FFAR1 signaling system could be decreased in chronic pain
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、ストレスにより誘発した慢性疼痛時の脳内では、リン脂質中の脂肪酸組成が低下していること、脂質関連因子が変化していることを見出した。これらの成果は、慢性疼痛時の脳内GPR40/FFAR1シグナル機構が機能低下している可能性を示している。したがって、将来的にこれら脂肪酸シグナルを標的とした新たな慢性疼痛治療薬の開発が期待される
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