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Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein

Author

Listed:
  • Martine Migaud

    (Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
    Centre for Neuroscience, University of Edinburgh)

  • Paul Charlesworth

    (Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
    Centre for Neuroscience, University of Edinburgh)

  • Maureen Dempster

    (Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
    Centre for Neuroscience, University of Edinburgh)

  • Lorna C. Webster

    (Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
    Centre for Neuroscience, University of Edinburgh)

  • Ayako M. Watabe

    (School of Medicine, University of California at Los Angeles)

  • Michael Makhinson

    (School of Medicine, University of California at Los Angeles)

  • Yong He

    (Fishberg Research Centre for Neurobiology, Mount Sinai School of Medicine)

  • Mark F. Ramsay

    (Centre for Neuroscience, University of Edinburgh)

  • Richard G. M. Morris

    (Centre for Neuroscience, University of Edinburgh)

  • John H. Morrison

    (Fishberg Research Centre for Neurobiology, Mount Sinai School of Medicine)

  • Thomas J. O'Dell

    (School of Medicine, University of California at Los Angeles)

  • Seth G. N. Grant

    (Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
    Centre for Neuroscience, University of Edinburgh)

Abstract

Specific patterns of neuronal firing induce changes in synaptic strength that may contribute to learning and memory. If the postsynaptic NMDA (N-methyl-D-aspartate) receptors are blocked, long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission and the learning of spatial information are prevented. The NMDA receptor can bind a protein known as postsynaptic density-95 (PSD-95), which may regulate the localization of and/or signalling by the receptor. In mutant mice lacking PSD-95, the frequency function of NMDA-dependent LTP and LTD is shifted to produce strikingly enhanced LTP at different frequencies of synaptic stimulation. In keeping with neural-network models that incorporate bidirectional learning rules, this frequency shift is accompanied by severely impaired spatial learning. Synaptic NMDA-receptor currents, subunit expression, localization and synaptic morphology are all unaffected in the mutant mice. PSD-95 thus appears to be important in coupling the NMDA receptor to pathways that control bidirectional synaptic plasticity and learning.

Suggested Citation

  • Martine Migaud & Paul Charlesworth & Maureen Dempster & Lorna C. Webster & Ayako M. Watabe & Michael Makhinson & Yong He & Mark F. Ramsay & Richard G. M. Morris & John H. Morrison & Thomas J. O'Dell &, 1998. "Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein," Nature, Nature, vol. 396(6710), pages 433-439, December.
    • Handle: RePEc:nat:nature:v:396:y:1998:i:6710:d:10.1038_24790
    DOI: 10.1038/24790
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    Cited by:

    1. Laura Tomas-Roca & Zhen Qiu & Erik Fransén & Ragini Gokhale & Edita Bulovaite & David J. Price & Noboru H. Komiyama & Seth G. N. Grant, 2022. "Developmental disruption and restoration of brain synaptome architecture in the murine Pax6 neurodevelopmental disease model," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    2. Nora Prochnow & Tina Gebing & Kerstin Ladage & Dorothee Krause-Finkeldey & Abdessamad El Ouardi & Andreas Bitz & Joachim Streckert & Volkert Hansen & Rolf Dermietzel, 2011. "Electromagnetic Field Effect or Simply Stress? Effects of UMTS Exposure on Hippocampal Longterm Plasticity in the Context of Procedure Related Hormone Release," PLOS ONE, Public Library of Science, vol. 6(5), pages 1-13, May.

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