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.
Highlights
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
Another important question is if given a choice, will oligodendroglial cells preferentially myelinate electrically active axons? In addition, oligodendrocytes are multipolar cells but it is unknown how different branches of the same oligodencrocyte are instructed by axons to act autonomously and selectively synthesize myelin in those processes that are in contact with active axons
The results indicate a strong preference for oligodendrocytes to myelinate electrically active axons via a mechanism dependent on nonsynaptic vesicular release of glutamate but independent of synapses on OPCs
Summary
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. 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. It has been shown that vesicular release of glutamate from axons stimulates local translation of myelin basic protein (MBP) and stimulates myelin induction[9] This signalling could be mediated by synaptic transmission or by spillover of neurotransmitter from axo-glial synapses activating extrasynaptic glutamate receptors on OPC processes[10,11]. To synaptic transmission, other forms of axo-glial communication could signal electrical activity in axons to OPCs. Nonsynaptic release of neurotransmitter operates by both vesicular and non-vesicular release mechanisms.
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