| Project/Area Number |
24792258
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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 |
Surgical dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
HONDA Kuniya 日本大学, 歯学部, ポスト・ドクトラル・フェロー (20548945)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 神経因性疼痛 / 痛覚過敏 / TRP channel / グルタミン酸受容体 / 代謝型グルタミン酸受容体 / TRPA1 / TRPV1 / PKC epsilon / 疼痛 |
|---|
| Research Abstract |
Peripheral tissue injury causes glutamate release from keratinocytes, resulting in hyperalgesia. We have reported that peripheral glutamate injection induces thermal hyperalgesia. However, it is still not understood the mechanisms underlying hyperalgesia following peripheral glutamate injection. To clarify the involvement of peripheral TRPA1, TRPV1 and PKC epsilon glutamate-induced hyperalgesia, we performed behavioral testing, immunohistochemistry and neuronal recording using glutamate injected rats. Present findings suggest that TRPA1 or TRPV1 activation through mGluR5 signaling via PKC epsilon is involved in facial thermal and mechanical hyperalgesia.
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