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

Hiroaki Wake, Fernando C. Ortiz, Dong Ho Woo, Philip R. Lee, María Cecilia Angulo and R. Douglas Fields ()
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Hiroaki Wake: Section on Nervous System Development and Plasticity, National Institutes of Health, National Institute of Child Health and Human Development
Fernando C. Ortiz: INSERM U1128
Dong Ho Woo: Section on Nervous System Development and Plasticity, National Institutes of Health, National Institute of Child Health and Human Development
Philip R. Lee: Section on Nervous System Development and Plasticity, National Institutes of Health, National Institute of Child Health and Human Development
María Cecilia Angulo: INSERM U1128
R. Douglas Fields: Section on Nervous System Development and Plasticity, National Institutes of Health, National Institute of Child Health and Human Development

Nature Communications, 2015, vol. 6, issue 1, 1-9

Abstract: Abstract 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.

Date: 2015
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DOI: 10.1038/ncomms8844

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