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Paranode Abnormalities and Oxidative Stress in Optic Nerve Vulnerable to Secondary Degeneration: Modulation by 670 nm Light Treatment.

Szymanski CR, Chiha W, Morellini N, Cummins N, Bartlett CA, O'Hare Doig RL, Savigni DL, Payne SC, Harvey AR, Dunlop SA, Fitzgerald M - PLoS ONE (2013)

Bottom Line: Concurrently, node of Ranvier/paranode complexes are altered, with significant lengthening of the paranodal gap and paranode as well as paranode disorganisation.Here, we show that light at 670 nm, delivered for 30 minutes per day, results in in vivo increases in cytochrome c oxidase activity co-localised with oligodendrocytes.Short term (1 day) 670 nm light treatment is associated with reductions in reactive species at the injury site.

View Article: PubMed Central - PubMed

Affiliation: Experimental and Regenerative Neurosciences, School of Animal Biology, The University of Western Australia, Crawley, Western Australia, Australia.

ABSTRACT
Secondary degeneration of nerve tissue adjacent to a traumatic injury results in further loss of neurons, glia and function, via mechanisms that may involve oxidative stress. However, changes in indicators of oxidative stress have not yet been demonstrated in oligodendrocytes vulnerable to secondary degeneration in vivo. We show increases in the oxidative stress indicator carboxymethyl lysine at days 1 and 3 after injury in oligodendrocytes vulnerable to secondary degeneration. Dihydroethidium staining for superoxide is reduced, indicating endogenous control of this particular reactive species after injury. Concurrently, node of Ranvier/paranode complexes are altered, with significant lengthening of the paranodal gap and paranode as well as paranode disorganisation. Therapeutic administration of 670 nm light is thought to improve oxidative metabolism via mechanisms that may include increased activity of cytochrome c oxidase. Here, we show that light at 670 nm, delivered for 30 minutes per day, results in in vivo increases in cytochrome c oxidase activity co-localised with oligodendrocytes. Short term (1 day) 670 nm light treatment is associated with reductions in reactive species at the injury site. In optic nerve vulnerable to secondary degeneration superoxide in oligodendrocytes is reduced relative to handling controls, and is associated with reduced paranode abnormalities. Long term (3 month) administration of 670 nm light preserves retinal ganglion cells vulnerable to secondary degeneration and maintains visual function, as assessed by the optokinetic nystagmus visual reflex. Light at a wavelength of 670 nm may serve as a therapeutic intervention for treatment of secondary degeneration following neurotrauma.

No MeSH data available.


Related in: MedlinePlus

Representative TEM images from normal ventral ON (a) and from day 1 after injury (b–d).Note the disorganisation, lack of definition (arrow head) and multi – layering (arrows) in the paranodal loops from ON vulnerable to secondary degeneration (b, c) and the complete breakdown in structure of one paranode in a node/paranode complex (d), scale bar  = 0.5 μm.
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pone-0066448-g003: Representative TEM images from normal ventral ON (a) and from day 1 after injury (b–d).Note the disorganisation, lack of definition (arrow head) and multi – layering (arrows) in the paranodal loops from ON vulnerable to secondary degeneration (b, c) and the complete breakdown in structure of one paranode in a node/paranode complex (d), scale bar  = 0.5 μm.

Mentions: Structural integrity of the node/paranode complex was also directly assessed using TEM, thereby providing information on the contacts of oligodendrocytes to the axon at the axoglial junction. Paranodes in normal ventral ON were characterised by defined paranodal loops in compact array (Fig. 3a). In contrast, in ventral ON at 1 day after injury, there was a pronounced disorganisation of the paranodal structure with many paranodal loops ill – defined and/or multilayered (Fig. 3b, c). Furthermore, in support of our immunohistochemical detection of hemi – nodes and single paranodes in ON vulnerable to secondary degeneration, we observed instances where one paranode was highly disrupted (Fig. 3d), likely reflecting a loss of immunoreactivity and associated functional disturbance.


Paranode Abnormalities and Oxidative Stress in Optic Nerve Vulnerable to Secondary Degeneration: Modulation by 670 nm Light Treatment.

Szymanski CR, Chiha W, Morellini N, Cummins N, Bartlett CA, O'Hare Doig RL, Savigni DL, Payne SC, Harvey AR, Dunlop SA, Fitzgerald M - PLoS ONE (2013)

Representative TEM images from normal ventral ON (a) and from day 1 after injury (b–d).Note the disorganisation, lack of definition (arrow head) and multi – layering (arrows) in the paranodal loops from ON vulnerable to secondary degeneration (b, c) and the complete breakdown in structure of one paranode in a node/paranode complex (d), scale bar  = 0.5 μm.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3686728&req=5

pone-0066448-g003: Representative TEM images from normal ventral ON (a) and from day 1 after injury (b–d).Note the disorganisation, lack of definition (arrow head) and multi – layering (arrows) in the paranodal loops from ON vulnerable to secondary degeneration (b, c) and the complete breakdown in structure of one paranode in a node/paranode complex (d), scale bar  = 0.5 μm.
Mentions: Structural integrity of the node/paranode complex was also directly assessed using TEM, thereby providing information on the contacts of oligodendrocytes to the axon at the axoglial junction. Paranodes in normal ventral ON were characterised by defined paranodal loops in compact array (Fig. 3a). In contrast, in ventral ON at 1 day after injury, there was a pronounced disorganisation of the paranodal structure with many paranodal loops ill – defined and/or multilayered (Fig. 3b, c). Furthermore, in support of our immunohistochemical detection of hemi – nodes and single paranodes in ON vulnerable to secondary degeneration, we observed instances where one paranode was highly disrupted (Fig. 3d), likely reflecting a loss of immunoreactivity and associated functional disturbance.

Bottom Line: Concurrently, node of Ranvier/paranode complexes are altered, with significant lengthening of the paranodal gap and paranode as well as paranode disorganisation.Here, we show that light at 670 nm, delivered for 30 minutes per day, results in in vivo increases in cytochrome c oxidase activity co-localised with oligodendrocytes.Short term (1 day) 670 nm light treatment is associated with reductions in reactive species at the injury site.

View Article: PubMed Central - PubMed

Affiliation: Experimental and Regenerative Neurosciences, School of Animal Biology, The University of Western Australia, Crawley, Western Australia, Australia.

ABSTRACT
Secondary degeneration of nerve tissue adjacent to a traumatic injury results in further loss of neurons, glia and function, via mechanisms that may involve oxidative stress. However, changes in indicators of oxidative stress have not yet been demonstrated in oligodendrocytes vulnerable to secondary degeneration in vivo. We show increases in the oxidative stress indicator carboxymethyl lysine at days 1 and 3 after injury in oligodendrocytes vulnerable to secondary degeneration. Dihydroethidium staining for superoxide is reduced, indicating endogenous control of this particular reactive species after injury. Concurrently, node of Ranvier/paranode complexes are altered, with significant lengthening of the paranodal gap and paranode as well as paranode disorganisation. Therapeutic administration of 670 nm light is thought to improve oxidative metabolism via mechanisms that may include increased activity of cytochrome c oxidase. Here, we show that light at 670 nm, delivered for 30 minutes per day, results in in vivo increases in cytochrome c oxidase activity co-localised with oligodendrocytes. Short term (1 day) 670 nm light treatment is associated with reductions in reactive species at the injury site. In optic nerve vulnerable to secondary degeneration superoxide in oligodendrocytes is reduced relative to handling controls, and is associated with reduced paranode abnormalities. Long term (3 month) administration of 670 nm light preserves retinal ganglion cells vulnerable to secondary degeneration and maintains visual function, as assessed by the optokinetic nystagmus visual reflex. Light at a wavelength of 670 nm may serve as a therapeutic intervention for treatment of secondary degeneration following neurotrauma.

No MeSH data available.


Related in: MedlinePlus