Project/Area Number |
22600009
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
疼痛学
|
Research Institution | Tohoku Pharmaceutical University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
MIZOGUCHI Hirokazu 東北薬科大学, 薬学部, 准教授 (30360069)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 癌性疼痛 / 鎮痛 / オピオイドペプチド / μ受容体 / ジーンセラピー |
Research Abstract |
Using a mouse model for neuropathic cancer pain, we found that the antinociceptive effects of morphine, oxycodone and methadone were markedly suppressed inthe neuropathic cancer pain. We also found that the antinociceptive effects of morphine, fentanyl and oxycodone are mediated through the activation ofμ-opioid receptor splice variants containing the sequences encoded by exon -1 or exon-4, whereas the antinociceptive effect of amidino-TAPA, which is a new analgesic effective against neuropathic pain, is mediated through the activation of μ -opioid receptor splice variants containing the sequences encoded by exon-1, exon-4, exon-12, exon-13orexon-14.
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