| Project/Area Number |
11680652
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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 |
Biophysics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KAWAHARA Shigenori The University of Tokyo, Graduate School of Pharmaceutical Sciences, Assistant Professor, 大学院・薬学系研究科, 助教授 (10204752)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | eyeblink / classical conditioning / learning / mouse / cerebellum / hippocampus / long-term depression |
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| Research Abstract |
The classical conditioning of the eyeblink response is a type of motor learning and critically depends on the cerebellum. In addition to the cerebellum, the hippocampus is also involved in this motor learning. We investigated the role of the hippocampus in the cerebellar long-term depression (LTD)-deficient mice that Jack the glutamate receptor subunit δ2 (GluRδ2). These mutant mice do not learn the delay eyeblink conditioning with CS-US overlap but learn the eyeblink conditioning with no CS-US overlap as successfully as the wild type mice. The hippocampally lesioned mutant mice, receiving aspiration of hippocampus and the overlying cortex, showed a severe impairment in eyeblink conditioning with no CS-US overlap, while the control mutant mice, receiving aspiration of the overlying cortex, did not. The hippocampally lesioned wild type mice learned as successfully as the control wild type mice. These results indicated that the hippocampus plays an important role in the LTD-independent learning mechanism observed in the GluRδ2 mutant mice.
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