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Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A

Author

Listed:
  • Saumya Das

    (Harvard Medical School)

  • Yasnory F. Sasaki

    (Harvard Medical School)

  • Thomas Rothe

    (Cerebrovascular and NeuroScience Research Institute, Neurosurgical Service, Brigham and Women's Hospital)

  • Louis S. Premkumar

    (State University of New York)

  • Mari Takasu

    (Harvard Medical School)

  • James E. Crandall

    (The Shriver Center for Mental Retardation
    Program in Neuroscience, Harvard Medical School)

  • Pieter Dikkes

    (Children's Hospital)

  • David A. Conner

    (Harvard Medical School)

  • Posina V. Rayudu

    (Cerebrovascular and NeuroScience Research Institute, Neurosurgical Service, Brigham and Women's Hospital)

  • Wing Cheung

    (Cerebrovascular and NeuroScience Research Institute, Neurosurgical Service, Brigham and Women's Hospital)

  • H.-S. Vincent Chen

    (Cerebrovascular and NeuroScience Research Institute, Neurosurgical Service, Brigham and Women's Hospital)

  • Stuart A. Lipton

    (Cerebrovascular and NeuroScience Research Institute, Neurosurgical Service, Brigham and Women's Hospital
    Program in Neuroscience, Harvard Medical School)

  • Nobuki Nakanishi

    (Harvard Medical School
    Program in Neuroscience, Harvard Medical School)

Abstract

The NMDA (N -methyl-D-aspartate) subclass of glutamate receptor1 is essential for the synaptic plasticity thought to underlie learning and memory2,3,4 and for synaptic refinement during development5,6. It is currently believed that the NMDA receptor (NMDAR) is a heteromultimeric channel comprising the ubiquitous NR1 subunit and at least one regionally localized NR2 subunit7,8,9,10,11. Here we report the characterization of a regulatory NMDAR subunit, NR3A (formerly termed NMDAR-L or χ-1), which is expressed primarily during brain development12,13. NR3Aco-immunoprecipitates with receptor subunits NR1 and NR2 in cerebrocortical extracts. In single-channel recordings from Xenopus oocytes, addition of NR3A to NR1 and NR2 leads to the appearance of a smaller unitary conductance. Genetic knockout of NR3A in mice results in enhanced NMDA responses and increased dendritic spines in early postnatal cerebrocortical neurons. These data suggest that NR3A is involved in the development of synaptic elements by modulating NMDAR activity.

Suggested Citation

  • Saumya Das & Yasnory F. Sasaki & Thomas Rothe & Louis S. Premkumar & Mari Takasu & James E. Crandall & Pieter Dikkes & David A. Conner & Posina V. Rayudu & Wing Cheung & H.-S. Vincent Chen & Stuart A., 1998. "Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A," Nature, Nature, vol. 393(6683), pages 377-381, May.
    • Handle: RePEc:nat:nature:v:393:y:1998:i:6683:d:10.1038_30748
    DOI: 10.1038/30748
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