| Project/Area Number |
17K10047
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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 |
Pediatrics
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| Research Institution | Akita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
高橋 勉 秋田大学, 医学系研究科, 教授 (20270845)
尾野 恭一 秋田大学, 医学系研究科, 教授 (70185635)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Nav1.9 / SCN11A / 小児四肢疼痛発作症 / ノックインマウス / 遺伝子改変マウス / ピエゾ素子式心拍呼吸モニタリング / ナトリウムチャネル / 発作性疼痛 / 遺伝性 / 痛みモニター |
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| Outline of Final Research Achievements |
The activity of NaV1.9 gene knock-in (KI) mice in low temperature and low atmospheric environments was quantified by an experimental momentum measuring device. In the comparison between the normal temperature (20-26℃) and the low temperature (15℃), the nighttime activity increased under the low temperature, which was more remarkable in KI mice (p<0.05). It was speculated that the hypersensitivity of KI mice to environmental temperature resulted in behavioral alterations. On the other hand, the nighttime activity amount decreased under +0.1 and -0.1 atm compared with the normal atmospheric pressure. This decrease was stronger in the KI mice group under -0.1 atmosphere (p<0.05). The behavioral changes of KI mice showed the opposite reaction in the low pressure environment and the low temperature environment, and it was verified that the reactivity to the low temperature and low pressure was significantly enhanced in the KI mouse group in both.
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| Academic Significance and Societal Importance of the Research Achievements |
最近明らかになった「Nav1.9変異による遺伝性疼痛疾患」を基盤として、そのマウスモデルの行動観察を行うことにより、疾患モデルとして環境が誘導する疼痛発作の機序を解明することは、「痛み」という元来数値化可視化し難かった徴候をある程度客観的に評価でき、これまで不明だった低気圧や寒冷刺激と疼痛の関係性を知る手がかりになる可能性がある。またNav1.9遺伝子改変マウスにおいて、1)疼痛発作の誘導、2)疼痛発作のモニター、が確立できれば、新たな疼痛研究ユニット（実験系）として、疼痛制御、疼痛創薬などに繋がる可能性が高い。
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