2014 Fiscal Year Final Research Report
Mechanism of mu opioid receptor agonist-evoked itch and effects of gabapentin on MOR agonist-induced itch
| Project/Area Number |
23590711
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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 |
Pain science
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| Research Institution | Shimane University |
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Principal Investigator |
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| Research Collaborator |
NARAI Yasuhiro
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Keywords | 痒み / 脊髄くも膜下腔 / オピオイド / ガバペンチン |
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| Outline of Final Research Achievements |
Although the mechanisms that underlie the production of itch are poorly understood, pruritis is a significant problem associated with analgesic therapies directed at the spinal cord. We showed μ opioid receptor(MOR) agonist-evoked itch is significantly reduced in the β3 isozyme of phospholipase C(PLCβ3) mutant mice.We are presently evaluating the contribution of PLCβ3 to the pruritis produced by MOR agonist administered directly to the spinal cord.
There is little information regarding its antipruritic effects of gabapentin (GBP).Intrathecally, GBP inhibited scratching behavior induced by DAMGO without reducing analgesic effect in mice. Our results suggest that intrathecal administration of GBP can be useful in reducing pruritis, while retaining its analgesic effects. In addition, we showed GBP and NSAIDs play an important role at the spinal level, and that GBP augments the antihyperalgesic effects induced by NSAIDs through a spinal action during the postoperative pain process.
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| Free Research Field |
麻酔科学
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