| Project/Area Number |
23790641
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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 | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KANEKO Shuji 京都大学, 大学院・薬学研究科, 教授 (60177516)
SHIRAKAWA Hisashi 京都大学, 大学院・薬学研究科, 助教 (50402798)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 疼痛の発生・増強機序 / 神経障害性疼痛 / TRP チャネル / TRPM2 / 免疫系細胞 / グリア細胞 / 脊髄 / 中枢性感作 / 慢性疼痛 / ミクログリア / マクロファージ / 神経炎症応答 / TRPC3 / アストロサイト / TRPV4 |
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| Research Abstract |
Chronic pain, such as peripheral nerve injury-induced neuropathic pain, is based on both peripheral and central sensitization, which is caused by neuroinflammation mediated by the interaction between peripheral/spinal neurons and immune/glial cells. In this research, we found that transient receptor potential (TRP) channels expressed in immune/glial cells play an important role in chronic pain. Especially, we examined the roles of TRPM2, which acts as a sensor for reactive oxygen species (ROS) in macrophages and microglia, in inflammatory and neuropathic pain in mice
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