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Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter

Nature Neuroscience volume 11, pages 450–456 (2008)Cite this article

A Corrigendum to this article was published on 01 July 2008

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Abstract

A defining feature of glial cells has been their inability to generate action potentials. We show here that there are two distinct types of morphologically identical oligodendrocyte precursor glial cells (OPCs) in situ in rat CNS white matter. One type expresses voltage-gated sodium and potassium channels, generates action potentials when depolarized and senses its environment by receiving excitatory and inhibitory synaptic input from axons. The other type lacks action potentials and synaptic input. We found that when OPCs suffered glutamate-mediated damage, as occurs in cerebral palsy, stroke and spinal cord injury, the action potential–generating OPCs were preferentially damaged, as they expressed more glutamate receptors, and received increased spontaneous glutamatergic synaptic input in ischemia. These data challenge the idea that only neurons generate action potentials in the CNS and imply that the development of therapies for demyelinating disorders will require defining which OPC type can carry out remyelination.

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Figure 1: Oligodendrocyte precursor identification.
Figure 2: Two classes of oligodendrocyte precursor glia.
Figure 3: Oligodendrocyte precursors proliferate, but do not label for astrocyte or neuronal markers.
Figure 4: Oligodendrocyte precursor glia with Na+ current generate action potentials.
Figure 5: Oligodendrocyte precursor glia with and without INa sense the environment differently.
Figure 6: Oligodendrocyte precursor glia with and without INa respond differently to ischemia.

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Change history

  • 21 May 2008

    In the version of this article initially published, the units for the values reported for resistance in Figure 2i,j were incorrect. The correct unit should be gigaohms. In addition, the authors did not state that the cell death experiments in Figure 6e,f were carried out using a physiological extracellular magnesium concentration of 1 mM. This error has been corrected in the HTML and PDF versions of the article.

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Acknowledgements

We thank W. Stallcup (Burnham Institute) for NG2 antibody, D. Rowitch, C.D. Stiles and J. Alberta (Harvard University) for Olig2 antibody, and R. Mirsky, K. Jessen, L. Jimenes-Diaz, S. Rakic, C. Eder, P. Mobbs, G. Frugier, A. Silver, A. Gibb and S. Bolsover for other antibodies, tissue and advice. This work was supported by the Wellcome Trust, a Wolfson-Royal Society Award to D.A. and a Royal Society Dorothy Hodgkin Fellowship to R.K.

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  1. Ragnhildur Káradóttir

    Present address: Present address: Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK.,

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  1. Department of Physiology, University College London, Gower Street, WC1E 6BT, London, UK

    Ragnhildur Káradóttir, Nicola B Hamilton, Yamina Bakiri & David Attwell

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Correspondence to Ragnhildur Káradóttir.

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Káradóttir, R., Hamilton, N., Bakiri, Y. et al. Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter. Nat Neurosci 11, 450–456 (2008). https://doi.org/10.1038/nn2060

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