| Project/Area Number |
18K08876
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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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| Review Section |
Basic Section 55050:Anesthesiology-related
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 慢性疼痛 / 電位依存性ナトリウムチャネル / 新たな鎮痛薬開発 / Nav1.9 / 新たな鎮痛薬 / Nav1.9抑制機序 / 選択的Nav1.9阻害薬 |
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| Outline of Final Research Achievements |
We planed the experiments that will elucidate the mechanisms underlying Nav1.9 inhibition to contribute development of selective Nav1.9 inhibitor for refractory chronic pain, however, we failed to express Nav1.9 in Xenopus oocytes for analysis. Therefore, we investigated the effects of some drugs that can be novel analgesics on the other sodium channel alpha subunits, using electrophysiological technique. We found that psychotropic drug, chlorpromazine, antitussive drug, carbetapentane and benzonatate inhibit the function of sodium channel alpha subunits that express in neuronal tissue including Nav1.2, Nav1.3, Nav1.6, Nav1.7, Nav1.8, dose-dependently. These results would indicate the possibility that these drugs will be novel analgesics for refractory chronic pain.
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| Academic Significance and Societal Importance of the Research Achievements |
炎症性疼痛や神経障害性疼痛を成因とする慢性疼痛は治療困難な例が多く、有効な鎮痛薬を開発すべく慢性疼痛の病態について研究が進められてきたが、未だ開発には至っていない。電位依存性ナトリウムチャネル（Nav）は慢性疼痛発生機序に重要な役割を持つことが示されており、向精神薬クロルプロマジンや鎮咳薬カルベタペンテン、ベンゾナテートが神経系に発現するNavサブユニット機能を抑制するという今回の発見は、これら薬物が難治性慢性疼痛に対する新たな鎮痛薬になり得る可能性を示唆している。
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