Journal
JOURNAL OF NEUROSCIENCE
Volume 36, Issue 35, Pages 9186-9200Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1444-16.2016
Keywords
ERK MAP kinase; intracellular signaling; myelin; myelin plasticity; oligodendrocyte; remyelination
Categories
Funding
- National Institutes of Health [1S10OD016236-01, R01 NS091084]
- National Institutes of Health (National Multiple Sclerosis Society Career-Transition Fellowship)
- National Institutes of Health (National Institute on Deafness and Other Communication Disorders) [013048]
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Growing evidence shows that mechanisms controlling CNS plasticity extend beyond the synapse and that alterations in myelin can modify conduction velocity, leading to changes in neural circuitry. Although it is widely accepted that newly generated oligodendrocytes (OLs) produce myelin in the adult CNS, the contribution of preexisting OLs to functional myelin remodeling is not known. Here, we show that sustained activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in preexisting OLs of adult mice is sufficient to drive increased myelin thickness, faster conduction speeds, and enhanced hippocampal-dependent emotional learning. Although preexisting OLs do not normally contribute to remyelination, we show that sustained activation of ERK1/2 renders them able to do so. These data suggest that strategies designed to push mature OLs to reinitiate myelination may be beneficial both for enhancing remyelination in demyelinating diseases and for increasing neural plasticity in the adult CNS.
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