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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

Longitudinal/transverse/oblique sections of uninjured optic nerve fibers fixed and processed using the pyroantimonate procedure to localize free calcium. Scattered along the length of the myelin sheaths of nerve fibers are foci of oval profiles at which myelin lamellae are separated such that individual lamellae are visible. These represent myelin discontinuities (md) (white arrows). Within several mds electron dense pyroantimonate precipitate occurs (black arrows) indicating the occurrence of free calcium therein. Mitochondria (mt) with a characteristic cristate ultrastructure and longitudinally orientate microtubules (double arrows) occur within the axoplasm.
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brainsci-03-01374-f004: Longitudinal/transverse/oblique sections of uninjured optic nerve fibers fixed and processed using the pyroantimonate procedure to localize free calcium. Scattered along the length of the myelin sheaths of nerve fibers are foci of oval profiles at which myelin lamellae are separated such that individual lamellae are visible. These represent myelin discontinuities (md) (white arrows). Within several mds electron dense pyroantimonate precipitate occurs (black arrows) indicating the occurrence of free calcium therein. Mitochondria (mt) with a characteristic cristate ultrastructure and longitudinally orientate microtubules (double arrows) occur within the axoplasm.

Mentions: A group of uninjured and injured animals were fixed and processed to localize free calcium ions by use of the modified pyroantimonate precipitation procedure [15,16,17]. In uninjured animals, small oval foci of separation of myelin lamellae form myelin discontinuities (Figure 4) and within some of these aggregates of pyroantimonate precipitate mark the presence of free calcium ions (Figure 4).


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

Maxwell WL - Brain Sci (2013)

Longitudinal/transverse/oblique sections of uninjured optic nerve fibers fixed and processed using the pyroantimonate procedure to localize free calcium. Scattered along the length of the myelin sheaths of nerve fibers are foci of oval profiles at which myelin lamellae are separated such that individual lamellae are visible. These represent myelin discontinuities (md) (white arrows). Within several mds electron dense pyroantimonate precipitate occurs (black arrows) indicating the occurrence of free calcium therein. Mitochondria (mt) with a characteristic cristate ultrastructure and longitudinally orientate microtubules (double arrows) occur within the axoplasm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

brainsci-03-01374-f004: Longitudinal/transverse/oblique sections of uninjured optic nerve fibers fixed and processed using the pyroantimonate procedure to localize free calcium. Scattered along the length of the myelin sheaths of nerve fibers are foci of oval profiles at which myelin lamellae are separated such that individual lamellae are visible. These represent myelin discontinuities (md) (white arrows). Within several mds electron dense pyroantimonate precipitate occurs (black arrows) indicating the occurrence of free calcium therein. Mitochondria (mt) with a characteristic cristate ultrastructure and longitudinally orientate microtubules (double arrows) occur within the axoplasm.
Mentions: A group of uninjured and injured animals were fixed and processed to localize free calcium ions by use of the modified pyroantimonate precipitation procedure [15,16,17]. In uninjured animals, small oval foci of separation of myelin lamellae form myelin discontinuities (Figure 4) and within some of these aggregates of pyroantimonate precipitate mark the presence of free calcium ions (Figure 4).

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