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Competitive binding of α-actinin and calmodulin to the NMDA receptor

Author

Listed:
  • Michael Wyszynski

    (Massachusetts General Hospital and Harvard Medical School)

  • Jerry Lin

    (Massachusetts General Hospital and Harvard Medical School)

  • Anuradha Rao

    (Massachusetts General Hospital and Harvard Medical School)

  • Elizabeth Nigh

    (Massachusetts General Hospital and Harvard Medical School)

  • Alan H. Beggs

    (Massachusetts General Hospital and Harvard Medical School)

  • Ann Marie Craig

    (Massachusetts General Hospital and Harvard Medical School)

  • Morgan Sheng

    (Massachusetts General Hospital and Harvard Medical School)

Abstract

The mechanisms by which neurotransmitter receptors are immobilized at postsynaptic sites in neurons are largely unknown. The activity of NMDA (N-methyl-D-aspartate) receptors is mechanosensitive1 and dependent on the integrity of actin2, suggesting a functionally important interaction between NMDA receptors and the postsynaptic cytoskeleton. α-Actinin-2, a member of the spectrin/dystrophin family of actin-binding proteins, is identified here as a brain postsynaptic density protein that colocalizes in dendritic spines with NMDA receptors and the putative NMDA receptor-clustering molecule PSD-95. α-Actinin-2 binds by its central rod domain to the cytoplasmic tail of both NR1 and NR2B subunits of the NMDA receptor, and can be immunoprecipitated with NMDA receptors and PSD-95 from rat brain. Intriguingly, NR1-α-actinin binding is directly antagonized by Ca2+/calmodulin. Thus α-actinin may play a role in both the localization of NMDA receptors and their modulation by Ca2+.

Suggested Citation

  • Michael Wyszynski & Jerry Lin & Anuradha Rao & Elizabeth Nigh & Alan H. Beggs & Ann Marie Craig & Morgan Sheng, 1997. "Competitive binding of α-actinin and calmodulin to the NMDA receptor," Nature, Nature, vol. 385(6615), pages 439-442, January.
    • Handle: RePEc:nat:nature:v:385:y:1997:i:6615:d:10.1038_385439a0
    DOI: 10.1038/385439a0
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