| Project/Area Number |
09480220
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KATSUKI Motoya The Institute of Medical Science, The University of Tokyo, Professor, 医科学研究所, 教授 (20051732)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAO Kazuki The Institute of Medical Science, The University of Tokyo, Visiting Research Ass, 医科学研究所, 寄付研究部門教員 (20217657)
NAKAMURA Kenji The Institute of Medical Science, The University of Tokyo, Research Associate, 医科学研究所, 助手 (90253533)
AIBA Atsu The Institute of Medical Science, The University of Tokyo, Associate Professor, 医科学研究所, 助教授 (20271116)
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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 |
¥13,200,000 (Direct Cost: ¥13,200,000)
Fiscal Year 1998: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 1997: ¥8,600,000 (Direct Cost: ¥8,600,000)
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| Keywords | animal models / pharmacology / dopamine receptor / brain function / gene targeting / gene replacement / ES cell / humanized mouse |
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| Research Abstract |
It is impossible to use human beings for the experimental studies of brain functions. Thus, we have to develop animal models for human brain functions. In human brain, dopamine is one of the key transmitters in the central nervous systems and is also suggested to control emotion, movement as well as various kinds of behaviors.
To elucidate the dopaminergic systems in the brain, we planned to generate dopamine receptor mutant mice, each of which lacks one of five dopamine (D1R-D5R) receptor genes. D1R, D2R and D4R mutant mouse lines were established by gene targeting and by intercrossing of the heterozygous mice, respectively. D4R and D2R mutant mice were crossed between them and the double mutant mice were obtained. These mice appeared very quiet and relatively smaller than the D2R or D4R mutant mice, probably because of the hortage of the appetite. The obvious abnormal behavior was also observed in these mutant mice.
The D3R and D5R mutant mice have yet to be obtained, though the ES cell lines, each gene of which had been already disrupted and the chimeric mice were also obtained. These mice will be established soon.
We are trying to elucidate the physiological functions of each dopamine receptor by pharmaco-behavioral experiments and by producing double and triple(or more)mutant mice as well.
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