title: Near infrared light reduces oxidative stress and preserves function in CNS tissue vulnerable to secondary degeneration following partial transection of the optic nerve.
abstract: Traumatic injury to the central nervous system (CNS) is accompanied by the spreading damage of secondary degeneration, resulting in further loss of neurons and function. Partial transection of the optic nerve (ON) has been used as a model of secondary degeneration, in which axons of retinal ganglion cells in the ventral ON are spared from initial dorsal injury, but are vulnerable to secondary degeneration. We have recently demonstrated that early after partial ON injury, oxidative stress spreads through the ventral ON vulnerable to secondary degeneration via astrocytes, and persists in the nerve in aggregates of cellular debris. In this study, we show that diffuse transcranial irradiation of the injury site with far red to near infrared (NIR) light (WARP 10 LED array, center wavelength 670 nm, irradiance 252 W/m(-2), 30 min exposure), as opposed to perception of light at this wavelength, reduced oxidative stress in areas of the ON vulnerable to secondary degeneration following partial injury. The WARP 10 NIR light treatment also prevented increases in NG-2-immunopositive oligodendrocyte precursor cells (OPCs) that occurred in ventral ON as a result of partial ON transection. Importantly, normal visual function was restored by NIR light treatment with the WARP 10 LED array, as assessed using optokinetic nystagmus and the Y-maze pattern discrimination task. To our knowledge, this is the first demonstration that 670-nm NIR light can reduce oxidative stress and improve function in the CNS following traumatic injury in vivo.
authors.affiliation: Experimental and Regenerative Neurosciences, The University of Western Australia, Crawley, Western Australia, Australia. lindy.fitzgerald@uwa.edu.au
authors.forename: Melinda
authors.initials: M
authors.lastname: Fitzgerald
authors.forename: Carole A
authors.initials: CA
authors.lastname: Bartlett
authors.forename: Sophie C
authors.initials: SC
authors.lastname: Payne
authors.forename: Nathan S
authors.initials: NS
authors.lastname: Hart
authors.forename: Jenny
authors.initials: J
authors.lastname: Rodger
authors.forename: Alan R
authors.initials: AR
authors.lastname: Harvey
authors.forename: Sarah A
authors.initials: SA
authors.lastname: Dunlop
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism; D001253:Astrocytes / Q000473:pathology / Q000528:radiation effects; D002490:Central Nervous System / Q000473:pathology* / Q000528:radiation effects*; D004192:Discrimination, Psychological / Q000502:physiology / Q000528:radiation effects; D005260:Female; D007150:Immunohistochemistry; D007259:Infrared Rays; D008264:Macrophages / Q000473:pathology; D017628:Microglia / Q000473:pathology; D008854:Microscopy, Electron; D009410:Nerve Degeneration / Q000473:pathology* / Q000532:radiotherapy*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D017120:Nystagmus, Optokinetic / Q000502:physiology; D009836:Oligodendroglia / Q000378:metabolism; D020221:Optic Nerve Injuries / Q000473:pathology* / Q000532:radiotherapy*; D018384:Oxidative Stress / Q000528:radiation effects*; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D014785:Vision, Ocular / Q000528:radiation effects; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D009419:Nerve Tissue Proteins; D011509:Proteoglycans; D013482:Superoxide Dismutase; D000099216:Chondroitin Sulfate Proteoglycan 4