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NMDA receptors are expressed in oligodendrocytes and activated in ischaemia

Author

Listed:
  • Ragnhildur Káradóttir

    (University College London)

  • Pauline Cavelier

    (University College London)

  • Linda H. Bergersen

    (University of Oslo)

  • David Attwell

    (University College London)

Abstract

Glial glutamate receptors Oligodendrocytes are the cells in the white matter of the central nervous system that produce and maintain the myelin sheath that insulates the impulse-carrying axon. They are damaged by the neurotransmitter glutamate in diseases as diverse as cerebral palsy, spinal cord injury, stroke and multiple sclerosis. It has become widely accepted that, unlike neurons which are mainly killed by glutamate acting on NMDA receptors, oligodendrocytes lack these receptors and are killed solely by glutamate acting on AMPA/kainate receptors. This thinking has guided therapeutic strategies, but it seems that the underlying assumption about glutamate receptor types may be wrong. Three papers published this week make a convincing case for the presence of NMDA receptors in oligodendrocytes, and for their involvement in causing damage to the cells in injury and disease. This will refocus attention on NMDA receptors as an important therapeutic target for drugs in a variety of neurological disorders.

Suggested Citation

  • Ragnhildur Káradóttir & Pauline Cavelier & Linda H. Bergersen & David Attwell, 2005. "NMDA receptors are expressed in oligodendrocytes and activated in ischaemia," Nature, Nature, vol. 438(7071), pages 1162-1166, December.
  • Handle: RePEc:nat:nature:v:438:y:2005:i:7071:d:10.1038_nature04302
    DOI: 10.1038/nature04302
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    Cited by:

    1. Chang Hoon Cho & Ilana Vasilisa Deyneko & Dylann Cordova-Martinez & Juan Vazquez & Anne S. Maguire & Jenny R. Diaz & Abigail U. Carbonell & Jaafar O. Tindi & Min-Hui Cui & Roman Fleysher & Sophie Molh, 2023. "ANKS1B encoded AIDA-1 regulates social behaviors by controlling oligodendrocyte function," Nature Communications, Nature, vol. 14(1), pages 1-20, December.

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