| Project/Area Number |
26500019
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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 |
Integrated Nutrition Science
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
加藤 伸郎 金沢医科大学, 医学部, 教授 (10152729)
谷口 真 金沢医科大学, 総合医学研究所, 講師 (30529433)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | イオンチャネル / 不飽和脂肪酸 / アミロイドベータ / アルツハイマー / 電気生理 |
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| Outline of Final Research Achievements |
We examined whether Slo1 BK channels were directly affected by Aβ1-42. Inside-out patch clamp recording revealed that soluble monomer Aβ1-42 had no effect on Slo1 BK channels heterologously expressed in HEK cells without intracellular Ca2+. Although Aβ1-42 oligomers reduced the channel current amplitude in some recordings, we could not conclude that Aβ1-42 affected Slo1 BK channels directly, because reproducibility of the results was scarce in this experimental condition. We also examined the effect of monomer and oligomers of Aβ1-42 on BK channels formed by Slo1 and the auxiliary subunit β1 or β4 expressed in HEK cells. Activity of Slo1 +β1 or Slo1 +β4 remained unaffected by monomer and oligomers of Aβ1-42.
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