| Project/Area Number |
21590280
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Hiroshima University |
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Principal Investigator |
NAKATA Yoshihiro 広島大学, 大学院・医歯薬学総合研究科, 教授 (40133152)
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| Research Collaborator |
MORIOKA Norimitsu 広島大学, 大学院・医歯薬学総合研究科, 講師 (20346505)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 知覚神経 / 神経ペプチド / 後根神経節細胞 / サブスタンスP / クロストーク / TRPA1 / dorsal root ganglion (DRG) / p38 MAPK / 疼痛制御機構 / allyl isothiocyanate (AITC) / ラジオイムノアッセイ / dorsal root ganglion(DRG) / allyl isothiocyanate(AITC) / マイクロダイアリシス法 / 線条体 / ホルマリン誘発性疼痛反応 / 麻薬性鎮痛薬 |
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| Research Abstract |
To examine mechanisms underlying substance P(SP) release from primary sensory neurons in response to activation of the nonselective cation channel transient receptor potential ankyrin 1(TRPA1), SP release from cultured rat dorsal root ganglion(DRG) neurons was measured, using radioimmunoassay, by stimulating TRPA1 with allyl isothiocyanate(AITC). The data suggest that activation of TRPA1 evokes SP release from the primary sensory neurons through phosphorylation of p38 MAP kinase, subsequent nociceptive behaviors and inflammatory responses. Furthermore, the data also indicate that blocking the effects in periphery tissue of TRPA1 activation leads to significant antinociception.
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