| Project/Area Number |
09044351
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | National Institute for Physiological Sciences |
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Principal Investigator |
IMOTO Keiji National Institute for Physiological Sciences, 生理学研究所, 教授 (00176512)
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| Co-Investigator(Kenkyū-buntansha) |
BEAM Kurt G Colorado State University Department of Anatomy & Neuroscience, 解剖・神経生物学教室, 教授
SCHWARTZ Arnold University of Cincinnati Institute of Molecular Pharamclogy, 分子薬理研究所, 所長
WAKAMORI Minoru National Institute for Physiological Sciences, 生理学研究所, 助手 (50222401)
NAKAI Junichi National Institute for Physiological Sciences, 生理学研究所, 助手 (80237198)
MORI Yasuo National Institute for Physiological Sciences, 生理学研究所, 助教授 (80212265)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥5,100,000 (Direct Cost: ¥5,100,000)
Fiscal Year 1998: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | calcium channel / gene targeting / neuronal conduction / neuronal transmission / action potenial |
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| Research Abstract |
We have characterized functional defects of the P/Q-type Ca2^<2+> channels induced by the ataxic mutations tottering (tg) and leaner (tg-la) in the pore-forming alpha_<14> (BI) subunit. Of these two mutations, tg-la which causes more sever ataxia affected biophysical properties of the P/Q-typeCa2^<2+> channel more seriously than the other. The stargazer gene whose mutation cause also epilepsy and ataxia was shown to encode a novel neuronal gamma isoform gamma_2. The interaction sites of the G protein subunits and intracellular Ca2^<2+> release channel (ryanodine receptor)were mapped in the cytoplasmic regions of the Ca2^<2+> channel alpha1 subunits.
In addition, we isolated a novel receptor-activated channel TRP5 from mouse brain. TRP5 was activated by receptor stimulation via a mechanism unrelated to store depletion.
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