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

Ragnhildur Káradóttir*, Nicola B. Hamilton, Yamina Bakiri, David Attwell

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

255 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)450-456
Number of pages7
JournalNature Neuroscience
Issue number4
Publication statusPublished - Apr 2008

Bibliographical note

Funding Information:
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.


Dive into the research topics of 'Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter'. Together they form a unique fingerprint.

Cite this