| Project/Area Number |
08610071
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
実験系心理学
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| Research Institution | University of Tsukuba |
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Principal Investigator |
IWASAKI Tsuneo Institute of Psychology University of Tsukuba, Professor, 心理学系, 教授 (70092509)
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| Co-Investigator(Kenkyū-buntansha) |
ICHITANI Yukio Institute of Psychology University of Tsukuba, Associate Professor, 心理学系, 助教授 (80176289)
YAMADA Kazuo Institute of Psychology University of Tsukuba, Research Associate, 心理学系, 助手 (30282312)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | learning / memory / striatum / acety1choline / gamma-aminobutyric acid / rat / ニコチン |
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| Research Abstract |
It is recently shown that the striatum (caudate-putamen) is associated with memory and learning processes. We have investigated in this study what neural circuit is concerned with performance of spatial memory tasks. Intrastriatal kainic acid administration producing neuronal cell death in the striatum caused severe deficits in radial arm maze and Morris water maze learning. On the other hand, intrastriatal injection of 6-hydroxydopamine, a selective catecholaminergic neurotoxin, did not have any clear disruptive effect on radial maze performance. These results suggest that neuronal cell bodies in the striatum are necessary for correct performance of these tasks while dopaminergic input into the striatum does not play an important role. We have further investigated whether learning deficits produced by intrastriatal kainic acid injection was ameliorated by systemic treatment of' agonists of gamma-aminobutyric acid (GABA) receptors and nicotinic acetyIcholine receptors. GABA-A receptor agonist significantly improved the radial maze performance in kainic acid-treated rats, but GABA-B receptor agonist did not. Nicotine, a nicotinic receptor agonist, did not have any effect on the performance. Results suggest that learning deficits in kainic acid-lesioned animals may partly come from the loss of striatal GABA neurons, and that a circuit containing GABA-A receptors in the brain plays an important role for the performance of radial maze task. The effect of muscarinic receptor agonist remains to be investigated in order to clarify the role of cholinergic receptors in the striatum.
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