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Molecularmechanism of motor learning

Research Project

Project/Area Number 12680745
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Neurochemistry/Neuropharmacology
Research InstitutionThe University of Tokyo

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)

Project Period (FY) 2000 – 2001
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥2,600,000 (Direct Cost: ¥2,600,000)
KeywordsGlutamate receptor / Gene knockout mice / Learning and memory / NMDA receptor / GluRδ2 / GluRδ / 遺伝子組み換え酵素Cre / グルタミン酸受容体チャネル / GluRδ2 / 小脳プルキンエ細胞 / LTD / 瞬目反射条件付け / GluRε1 / 海馬 / LTP
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.

Report

(3 results)
  • 2001 Annual Research Report   Final Research Report Summary
  • 2000 Annual Research Report
  • Research Products

    (21 results)

All Other

All Publications (21 results)

  • [Publications] Takatsuki, K. et al.: "Scopolamine impairs eyeblink conditioning in cerebellar LTD-deficient mice"NeuroReport. 13. 159-162 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Kishimoto, Y. et al.: "Impairment of eyeblink conditioning in GluRδ2 mutant mice depends on the temporal overlap between conditioned and unconditioned stimuli"Fur. J. Neurosci.. 14. 1515-1521 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Takeuchi, T. et al.: "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(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Kishimoto, Y. et al.: "Long-trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit ε1"Eur. J. Neurosci.. 13. 1221-1227 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Kishimoto, Y. et al.: "Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in the delay paradigm but not in the trace paradigm"Eur. J. Neurosci.. 13. 1249-1253 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Takatsuki K, Kawahara S, Mori H, Mishina M, Kirino Y.: "Scopolamine impairs eyeblink conditioning in cerebellar LTD-deficient mice"NeuroRepoprt. 13. 159-162 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Kishimoto Y, Kawahara S, Fujimichi R, Mori H, Mishina M, Kirino Y.: "Impairment of eyeblink conditioning in GluRδ2 mutant mice depends on the temporal overlap between conditioned and unconditioned stimuli"Eur. J. Neurosci. 14. 1515-1521 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Kishimoto Y, Kawahara S, Mori H, Mishina M, Kirino Y.: "Long-trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit ε1"Eur. J. Neurosci.. 13. 1221-1227 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Kishimoto Y, Kawahara S, Suzuki M, Mori H, Mishina M, Kirino Y.: "Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in the delay paradigm but not in the trace paradigm"Eur. J. Neurosci.. 13. 1249-1253 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Miyamoto Y, Yamada K, Noda Y, Mori H, Mishina M, Nabeshima T.: "Hyperfunction of dopaminergic and serotonergic neuronal systems in mice lacking the NMDA receptor ε1 subunit"J. Neurosci. 21. 750-757 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Takatsuki, K. et al.: "Scopolamine impairs eyeblink conditioning in cerebellar LTD-deficient mice"NeuroReport. 13. 159-162 (2002)

    • Related Report
      2001 Annual Research Report
  • [Publications] Kishimoto, Y. et al.: "Impairment eyeblink conditioning in GluRδ2 mutant mice depends on the temporal overlap between conditioned and unconditioned stimuli"Eur. J. Neurosci.. 14. 1515-1521 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Takeuchi, T. et al.: "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)

    • Related Report
      2001 Annual Research Report
  • [Publications] Kishimoto, Y. et al.: "Long-trace interbal eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit ε1"Eur. J. Neurosci.. 13. 1221-1227 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Kishimoto, Y. et al.: "Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in the delay paradigm but not in the trace paradigm"Eur. J. Neurosci.. 13. 1249-1253 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Nakamura,K et al.,: "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)

    • Related Report
      2000 Annual Research Report
  • [Publications] Miyamoto,Y et al.,: "Hyperfunction of dopaminergic and serotonergic neural systems in mice lacking NMDA receptor ε1 subunit."J.Neurosci.. 21. 750-757 (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] Kishimoto,Y et al.,: "Long-trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit ε1"Eur.J.Neurosci. 13. 1221-1227 (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] Kishimoto Y. et al.,: "Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in the delay paradigm but not in the trace paradigm."Eur.J.Neurosci.. 13. 1249-1253 (2001)

    • Related Report
      2000 Annual Research Report

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Published: 2000-04-01   Modified: 2016-04-21  

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