| Project/Area Number |
16K09004
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | Hyogo University of Health Sciences |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
田中 康一 兵庫医療大学, 薬学部, 講師 (30274848)
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| Research Collaborator |
DAI Tsuyoshi
KOGURE Yoko
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 神経因性疼痛 / 脊髄後根神経節 / Kチャネル / 熱 / セロトニン / セロトニン受容体 / 神経傷害性疼痛 / K+チャネル / TRPV1受容体 / 神経障害性疼痛 / 神経科学 |
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| Outline of Final Research Achievements |
To study the mechanism of generation of neuropathic pain, a role of serotonin on a novel heat-activated K channel (Kheat) in dorsal root ganglion neurons of the rat was examined using a patch-clamp technique. Kheat was isolated by Ba or tetraethylammonium. Under the isolation of Kheat, serotonin did not affect to Kheat, as well as to TRPV1 receptors.
The reason of the less effect of serotonin might be attribute to using normal rats but not neuropathic pain model rats in this study. To clear the problem, similar experiments will be continue in neuropathic pain model rats.
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| Academic Significance and Societal Importance of the Research Achievements |
末梢神経傷害後に発生する神経因性疼痛は，創傷治癒後に持続する難治性疾患である。この疼痛に関与する分子としてATP，セロトニンやノルアドレナリン(NA)などの化学伝達物質，TRPV1受容体やセロトニン受容体(5-HT受容体)などが挙げられている。これまでに我々は，神経因性疼痛の発生メカニズムとして，NAと熱感受性Kチャネル(Kheatチャネル)の関係を明らかにしてきた。今回の研究では，NAと同様に「セロトニンがKheatチャネルを抑制すれば疼痛発生の要因となる」と仮説を立て，それを実証する実験を行い，神経因性疼痛発生機序の解明に繋げる。
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