| Project/Area Number |
24790576
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pain science
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAGAI JUN 長崎大学, 医歯(薬)学総合研究科, 助教 (20608369)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 線維筋痛症 / リゾリン脂質 / LC-MS/MS / TOF-MS / 慢性疼痛 / 下降性抑制 / エピゲノム / オピオイド / リゾホスファチジン酸 / 質量分析 / 神経障害性疼痛 / プレガバリン / オピオイド受容体 / cPLA2 / iPLA2 / 質量分析定量 / マイクログリア / エピジェネティクス |
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| Research Abstract |
In fibromyalgia, using the intermittent cold stress (ICS) mouse model, the loss of descending activation system seems to be a key mechanism underlying the absence of morphine analgesia. In neuropathic pain, absence of morphine analgesia is induced by down-regulation of MOP gene through epigenetic silencing mechanism. In FM model, MOP gene level was not altered. On the other hand, it has long been known that lipid mediators are key regulators of pain perception. We have successfully established quantitative analytical methods for proalgesic and analgesic lipid mediators using LC-MS/MS and TOF-MS techniques. We quantified lipid mediator levels in the selected brain regions along the pain descending pathway. Our data did not indicate a significant alteration in the lipid levels of the brain regions investigated. These results suggest that fibromyalgia is different from the neuropathic pain, at least in terms of lipid metabolisms and epigenomic silencing mechanism.
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