Damage to myelin and oligodendrocytes: a role in chronic outcomes following traumatic brain injury?

Maxwell, W. L. (2013) Damage to myelin and oligodendrocytes: a role in chronic outcomes following traumatic brain injury? Brain Sciences, 3(3), pp. 1374-1394. (doi: 10.3390/brainsci3031374) (PMID:24961533) (PMCID:PMC4061868)

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There is increasing evidence in the experimental and clinical traumatic brain injury (TBI) literature that loss of central myelinated nerve fibers continues over the chronic post-traumatic phase after injury. However, the biomechanism(s) of continued loss of axons is obscure. Stretch-injury to optic nerve fibers in adult guinea-pigs was used to test the hypothesis that damage to the myelin sheath and oligodendrocytes of the optic nerve fibers may contribute to, or facilitate, the continuance of axonal loss. Myelin dislocations occur within internodal myelin of larger axons within 1–2 h of TBI. The myelin dislocations contain elevated levels of free calcium. The volume of myelin dislocations increase with greater survival and are associated with disruption of the axonal cytoskeleton leading to secondary axotomy. Waves of Ca2+ depolarization or spreading depression extend from the initial locus injury for perhaps hundreds of microns after TBI. As astrocytes and oligodendrocytes are connected via gap junctions, it is hypothesized that spreading depression results in depolarization of central glia, disrupt axonal ionic homeostasis, injure axonal mitochondria and allow the onset of axonal degeneration throughout an increasing volume of brain tissue; and contribute toward post-traumatic continued loss of white matter.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Maxwell, Dr William
Authors: Maxwell, W. L.
College/School:College of Medical Veterinary and Life Sciences > School of Life Sciences
Journal Name:Brain Sciences
ISSN (Online):2076-3425
Copyright Holders:Copyright © 2013 The Author
First Published:First published in Brain Sciences 3(3):1374-1394
Publisher Policy:Reproduced under a Creative Commons License

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