| Project/Area Number |
16K08629
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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 |
Pathological medical chemistry
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Research Collaborator |
Ikeda Keiko
Sugimoto Hiroki
Unekawa Miyuki
Suzuki Norihiro
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 家族性偏頭痛 / ナトリウムポンプ / カルシウムイメージング / 大脳皮質拡延性抑制 / CSD / Caイメージング / ナトリウムポンプα２サブユニット / 偏頭痛 / 家族性片麻痺性偏頭痛２型 / トランスジェニックマウス / ナトリウムポンプα3サブユニット / 片頭痛 / c-FOS |
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| Outline of Final Research Achievements |
1. The mice habouring mutation of E700K of Atp1a2, which has been identified as causative mutation of familial hemiplegic migraine, showed fast spreading of CSD and slow recovery from the potential drop. The threshold of CSD induction was lower in the female mutant mice.
2. We analyzed the change of Ca2+ concentration of neuron and astrocyte in vivo. (1) The number of astrocytes that showed the increment of Ca2+ concentration was higher in the Atp1a2 deficient mice. (2) The synchrony of intracellular Ca2+ concentration variation was significantly lower in the astrocytes of Atp1a2 deficient mice.
3. The expression of Iba-1, which is known as a marker of inflammation was augmented in the Atp1a2 deficient mice.
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| Academic Significance and Societal Importance of the Research Achievements |
これらにより、ヒト患者で見つかる変異を導入したマウスが、CSDの属性に変化をきたしており、偏頭痛のモデルとして有効であることを明らかにできた。これらの結果により、Atp1a2欠損マウスのアストロサイトでの機能的な変化が示唆された。
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