Journal
NEURON
Volume 91, Issue 4, Pages 824-836Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2016.07.021
Keywords
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Categories
Funding
- NMSS [RG4541A3, RG5203A4]
- NIH/NINDS [R01NS062796, R01NS097428, R01NS50220]
- Rachleff Family Professorship
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- Incumbent of the Hanna Hertz Professorial Chair for Multiple Sclerosis and Neuroscience
- NSERC PGS D
- NIH/NINDS Ruth L. Kirschstein NRSA [F31NS081905]
- Wellcome Trust [102836/Z/13/Z] Funding Source: researchfish
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Myelination occurs selectively around neuronal axons to increase the efficiency and velocity of action potentials. While oligodendrocytes are capable of myelinating permissive structures in the absence of molecular cues, structurally permissive neuronal somata and dendrites remain unmyelinated. Utilizing a purified spinal cord neuron-oligodendrocyte myelinating co-culture system, we demonstrate that disruption of dynamic neuron-oligodendrocyte signaling by chemical cross-linking results in aberrant myelination of the somatodendritic compartment of neurons. We hypothesize that an inhibitory somatodendritic cue is necessary to prevent non-axonal myelination. Using next-generation sequencing and candidate profiling, we identify neuronal junction adhesion molecule 2 (JAM2) as an inhibitory myelin-guidance molecule. Taken together, our results demonstrate that the somatodendritic compartment directly inhibits myelination and suggest a model in which broadly indiscriminate myelination is tailored by inhibitory signaling to meet local myelination requirements.
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