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Nat Commun. 2015 Aug 4;6:7844. doi: 10.1038/ncomms8844.

Nonsynaptic junctions on myelinating glia promote preferential myelination of electrically active axons.

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Section on Nervous System Development and Plasticity, National Institutes of Health, National Institute of Child Health and Human Development, Building 35, Room 2A211, MSC 3713, 35 Lincoln Drive, Bethesda, Maryland 20892, USA.
1] INSERM U1128, 75006 Paris, France [2] Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France.


The myelin sheath on vertebrate axons is critical for neural impulse transmission, but whether electrically active axons are preferentially myelinated by glial cells, and if so, whether axo-glial synapses are involved, are long-standing questions of significance to nervous system development, plasticity and disease. Here we show using an in vitro system that oligodendrocytes preferentially myelinate electrically active axons, but synapses from axons onto myelin-forming oligodendroglial cells are not required. Instead, vesicular release at nonsynaptic axo-glial junctions induces myelination. Axons releasing neurotransmitter from vesicles that accumulate in axon varicosities induces a local rise in cytoplasmic calcium in glial cell processes at these nonsynaptic functional junctions, and this signalling stimulates local translation of myelin basic protein to initiate myelination.

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