Journal
NATURE NEUROSCIENCE
Volume 11, Issue 4, Pages 450-456Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn2060
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Funding
- Medical Research Council [G0800784, G0300723] Funding Source: Medline
- Wellcome Trust [065424, 075232] Funding Source: Medline
- MRC [G0300723] Funding Source: UKRI
- Medical Research Council [G0300723, G0300723B] Funding Source: researchfish
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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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