Sunday, 12 April 2015

Nerve signalling facilitates myelination

Mensch S, Baraban M, Almeida R, Czopka T, Ausborn J, El Manira A, Lyons DA. Synaptic vesicle release regulates myelin sheath number of individual oligodendrocytes in vivo. Nat Neurosci. 2015 Apr 6. doi: 10.1038/nn.3991. [Epub ahead of print]

The myelination of axons by oligodendrocytes markedly affects CNS function, but how this is regulated by neuronal activity in vivo is not known. We found that blocking synaptic vesicle release impaired CNS myelination by reducing the number of myelin sheaths made by individual oligodendrocytes during their short period of formation. We also found that stimulating neuronal activity increased myelin sheath formation by individual oligodendrocytes. These data indicate that neuronal activity regulates the myelinating capacity of single oligodendrocytes.

period of stimulation at
Neuron A (transmitting) to neuron B(receiving).
1. Mitochondria;
2. Synaptic vesicle with neurotransmitters;
3. Autoreceptor
4. Synapse with neurotransmitter released (serotonin);
5. Postsynaptic receptors activated by neurotransmitter (induction of a postsynaptic potential);
6. Calcium channel;
7. Exocytosis of a vesicle;
8. Recaptured neurotransmitter


In a neuron, synaptic vesicles (or neurotransmitter vesicles) store various neurotransmitters that are relapsed at the synapse. The release is regulated by a voltage-dependent calcium channelVesicles are essential for propagating nerve impulses between neurons and are constantly recreated by the cell. The area in the axon that holds groups of vesicles is an axon terminal or "bouton".  
In this study the activity of the nerve determined the extent to which it was myelinated. It makes biological sense. 

It also makes you wonder what Levetiracetam (Keppra) a drug that modulates synaptic vesicle formation and has been tested in MS to control spasticity, pain, tremor seizures. I don't think there is any evidence it makes things worse and it didn't appear to inhibit demyelination.

1 comment:

  1. Why are some axons in the CNS unmyelinated? Is myelination due to the activity of the neuron or is it dependent on the diameter of the axon or whether a synaptic connection with another neuron is made? If activity is important to myelination does inactivity lead to demyelination or is this just applicable to development? Interesting post.

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