2001 Fiscal Year Final Research Report Summary
Molecularmechanism of motor learning
| Project/Area Number |
12680745
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MORI Hisashi Department of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, The University of Tokyo. Lecturer, 大学院・医学系研究科, 講師 (00239617)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Glutamate receptor / Gene knockout mice / Learning and memory / NMDA receptor / GluRδ2 / GluRδ |
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| Research Abstract |
To investigate the molecular mechanism of motor learning, we have analyzed the eyeblink conditioning in glutamate receptor (GluR) subunit gene knockout (KO) mice. We have used cerebellar Purkinje cell-specific GluRδ2 KO and NMDA-type GluRε1 KO mice. We have obtained following results.
1) We conducted the eyeblink conditioning with GluRδ2 KO mice, using various temporal intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). In the delay paradigm in which the CS overlapped temporally with US, GluRδ2 KO mice exhibited severe learning impairment. In contrast, GluRδ2 KO mice learned well the paradigm in which no temporal overlap between the CS and US. Because the GluRδ2 KO mice have deficient in cerebellar LTD, these results indicates the GluRδ2 and LTD are essential for motor learning when there is CS-US temporal overlap, suggesting that the cerebellar substrates underlying eyeblink conditioning may change, depending on the temporal overlap of the CS and US.
2) The NMDA-type GluRε1 KO mice exhibited sever learning impairment in eyeblink conditioning with a long trace interval between the CS and US. In contrast, these mice showed a little slow learning in the delay and short trace paradigms. These results indicate that the NMDA-type GluRε1 is essential for long-trace interval eyeblink conditioning.
3) We have also analyzed the acoustic startle response (ASR) of NMDA-type GluRε1 KO, GluRε2 KO, GluRε3 KO and GluRε4 KO mice. The GluRε2 hetero KO mice showed the enhancement of ASR. On the other hand, heterozygous and homozygous mutation of the other NMDA-type GluRε subunits exerted no, or only small effects on ASR. We suggest that the GluRε2 subunit play a distinct role in the regulation of the ASR.
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Research Products
(12 results)
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[Publications] Takeuchi T, Kiyama Y, Nakamura K, Tsujita M, Matsuda I, Mori H, Munemoto Y, Kuriyama H, Natsume R, Sakimura K, Mishina M.: "Roles of the glutamate receptor ε2 and δ2 subunits in the potentiation and prepulse inhibition of the acoustic startle reflex"Eur. J. Neurosci.. 14. 153-160 (2001)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Nakamura K, Manabe T, Watanabe M, Mamiya T, Ichikawa R, Kiyama Y, Sanbo M, Yagi T, Inoue Y, Nabeshima T, Mori H, Mishina M.: "Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon-specific cell adhesion molecule"Eur. J. Neurosci.. 13. 179-189 (2001)
Description
「研究成果報告書概要(欧文)」より
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