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

Maxwell WL - Brain Sci (2013)

Bottom Line: However, the biomechanism(s) of continued loss of axons is obscure.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Anatomy, College of Medicine, Veterinary Medicine and Biological Sciences, University of Glasgow, Glasgow G12 8QQ, UK. William.Maxwell@Glasgow.ac.uk.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

A low magnification, longitudinal plane field of a resin embedded thin section of optic nerve at 2 h after an acute stretch-injury (19–22 ms period of mechanical loading). Two astrocyte cell bodies (A) are visible. Bundles of astrocyte intermediate filaments (GFAP) (arrow) occur within astrocyte processes (black arrows) extending between myelinated nerve fibres. A large, damaged nerve fibre with a lucent axoplasm and numerous irregular myelin discontinuities (md—white arrows) is visible in the centre of this field. Closer examination of the field reveals numerous lucent and dark md in the myelin sheaths of neighboring, smaller nerve fibers (dotted white arrows). Magnification 2300×.
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brainsci-03-01374-f002: A low magnification, longitudinal plane field of a resin embedded thin section of optic nerve at 2 h after an acute stretch-injury (19–22 ms period of mechanical loading). Two astrocyte cell bodies (A) are visible. Bundles of astrocyte intermediate filaments (GFAP) (arrow) occur within astrocyte processes (black arrows) extending between myelinated nerve fibres. A large, damaged nerve fibre with a lucent axoplasm and numerous irregular myelin discontinuities (md—white arrows) is visible in the centre of this field. Closer examination of the field reveals numerous lucent and dark md in the myelin sheaths of neighboring, smaller nerve fibers (dotted white arrows). Magnification 2300×.

Mentions: The earliest changes in myelin morphology may be seen at 2 h after stretch-injury in the guinea-pig optic nerve model of TAI (Figure 2). At low magnification, numerous irregular myelin profiles occur within the myelin sheaths of large and small nerve fibers viewed in longitudinal section. In the present study these myelin profiles will be termed myelin discontinuities or (md) (Figure 2 white arrows).


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

Maxwell WL - Brain Sci (2013)

A low magnification, longitudinal plane field of a resin embedded thin section of optic nerve at 2 h after an acute stretch-injury (19–22 ms period of mechanical loading). Two astrocyte cell bodies (A) are visible. Bundles of astrocyte intermediate filaments (GFAP) (arrow) occur within astrocyte processes (black arrows) extending between myelinated nerve fibres. A large, damaged nerve fibre with a lucent axoplasm and numerous irregular myelin discontinuities (md—white arrows) is visible in the centre of this field. Closer examination of the field reveals numerous lucent and dark md in the myelin sheaths of neighboring, smaller nerve fibers (dotted white arrows). Magnification 2300×.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061868&req=5

brainsci-03-01374-f002: A low magnification, longitudinal plane field of a resin embedded thin section of optic nerve at 2 h after an acute stretch-injury (19–22 ms period of mechanical loading). Two astrocyte cell bodies (A) are visible. Bundles of astrocyte intermediate filaments (GFAP) (arrow) occur within astrocyte processes (black arrows) extending between myelinated nerve fibres. A large, damaged nerve fibre with a lucent axoplasm and numerous irregular myelin discontinuities (md—white arrows) is visible in the centre of this field. Closer examination of the field reveals numerous lucent and dark md in the myelin sheaths of neighboring, smaller nerve fibers (dotted white arrows). Magnification 2300×.
Mentions: The earliest changes in myelin morphology may be seen at 2 h after stretch-injury in the guinea-pig optic nerve model of TAI (Figure 2). At low magnification, numerous irregular myelin profiles occur within the myelin sheaths of large and small nerve fibers viewed in longitudinal section. In the present study these myelin profiles will be termed myelin discontinuities or (md) (Figure 2 white arrows).

Bottom Line: However, the biomechanism(s) of continued loss of axons is obscure.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Anatomy, College of Medicine, Veterinary Medicine and Biological Sciences, University of Glasgow, Glasgow G12 8QQ, UK. William.Maxwell@Glasgow.ac.uk.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus