| Project/Area Number |
25462458
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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
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| Research Institution | Kobe Gakuin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMOTO Kazuo 神戸学院大学, 薬学部, 講師 (30432636)
HARADA Shinichi 神戸学院大学, 薬学部, 講師 (60633443)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 脳卒中後疼痛 / 長鎖脂肪酸 / GPR40 / 全脳虚血ストレス / 脳虚血ストレス / 疼痛 / プロテオーム / 鎮痛補助薬 / アストロサイト / 全脳虚血モデル |
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| Outline of Final Research Achievements |
Central post-stroke pain (CPSP), one of the complications of cerebral ischemia and neuropathic pain syndrome, is associated with specific somatosensory abnormalities.We recently reported that DHA and/or GW9508, a GPR40 agonist, have suppressive effects on pain behavior elicited by formalin, acetic acid and a complete Freund's adjuvant. These effects appear to be mediated through the release of β-endorphin, an endogenous opioid peptide, which is stimulated by GPR40 signaling in the supraspinal region. The aim of the present study was to determine the involvement of GPR40 in the development of CPSP in an animal model of global cerebral ischemia. BCAO-induced mechanical hyperalgesia was significantly decreased by intracerebroventricular injection of docosahexaenoic acid or GW9508, a GPR40 agonist; furthermore, these effects were reversed by GW1100, a GPR40 antagonist.Our data show that BCAO-induced mechanical hyperalgesia can be regulated by stimulation of GPR40 signaling.
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