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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

Effects of 670 nm light on RGC numbers and visual function.Mean ± SEM retrograde labelled RGC numbers (central or ventral retinal regions) (a) and responses in the optokinetic nystagmus test of visual function (smooth pursuits or fast resets) (b), in 670 nm treated or control animals 3 months after injury, * significant differences indicated (p≤0.05) (n = 4–5 animals / group), PT is partial ON transection injury.
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pone-0066448-g008: Effects of 670 nm light on RGC numbers and visual function.Mean ± SEM retrograde labelled RGC numbers (central or ventral retinal regions) (a) and responses in the optokinetic nystagmus test of visual function (smooth pursuits or fast resets) (b), in 670 nm treated or control animals 3 months after injury, * significant differences indicated (p≤0.05) (n = 4–5 animals / group), PT is partial ON transection injury.

Mentions: It is important to know whether prevention of early paranode abnormalities and sustained long – term 670 nm treatments are associated with neuroprotection and preservation of function. As expected, there was a significant decrease in numbers of retrogradely labelled RGCs in central and ventral retina following injury (PT handled compared to handled normal, ventral retina, p = 0.012, dF  = 2, Fig. 8a). However, there was no significant loss of RGCs in central or ventral retinae following injury when animals were treated with the 670 nm light (PT 670 nm compared to handled normal, p>0.05). RGCs in central retinae are vulnerable to death from both the primary injury and from secondary degeneration, whereas RGCs in ventral retinae are vulnerable to death from exclusively secondary mechanisms [6]. As such, 670 nm light treatment limited the loss of RGCs vulnerable to secondary degeneration, particularly those in ventral retina (Fig. 8a). The lower numbers of retrogradely labelled RGCs in ventral compared to central retina of normal and of injured animals are as described [6].


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)

Effects of 670 nm light on RGC numbers and visual function.Mean ± SEM retrograde labelled RGC numbers (central or ventral retinal regions) (a) and responses in the optokinetic nystagmus test of visual function (smooth pursuits or fast resets) (b), in 670 nm treated or control animals 3 months after injury, * significant differences indicated (p≤0.05) (n = 4–5 animals / group), PT is partial ON transection injury.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3686728&req=5

pone-0066448-g008: Effects of 670 nm light on RGC numbers and visual function.Mean ± SEM retrograde labelled RGC numbers (central or ventral retinal regions) (a) and responses in the optokinetic nystagmus test of visual function (smooth pursuits or fast resets) (b), in 670 nm treated or control animals 3 months after injury, * significant differences indicated (p≤0.05) (n = 4–5 animals / group), PT is partial ON transection injury.
Mentions: It is important to know whether prevention of early paranode abnormalities and sustained long – term 670 nm treatments are associated with neuroprotection and preservation of function. As expected, there was a significant decrease in numbers of retrogradely labelled RGCs in central and ventral retina following injury (PT handled compared to handled normal, ventral retina, p = 0.012, dF  = 2, Fig. 8a). However, there was no significant loss of RGCs in central or ventral retinae following injury when animals were treated with the 670 nm light (PT 670 nm compared to handled normal, p>0.05). RGCs in central retinae are vulnerable to death from both the primary injury and from secondary degeneration, whereas RGCs in ventral retinae are vulnerable to death from exclusively secondary mechanisms [6]. As such, 670 nm light treatment limited the loss of RGCs vulnerable to secondary degeneration, particularly those in ventral retina (Fig. 8a). The lower numbers of retrogradely labelled RGCs in ventral compared to central retina of normal and of injured animals are as described [6].

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