Abstract
<h3>Research Objectives</h3> Traumatic optic neuropathy (TON) is a significant cause of visual impairment after head trauma and has few effective treatment options. In a mouse model of TON we previously noted post-injury apnea led to immediate mortality in adolescents and brief exposure to 100% oxygen reduced the mortality rate. We hypothesized that oxygen exposure may have an effect on the pathophysiology and functional deficits associated with TON and age at injury might modulate these effects. <h3>Design</h3> This was a randomized controlled preclinical intervention study of brief oxygen supplementation after experimental head trauma. Mice were followed for 7 days after injury. <h3>Setting</h3> Preclinical research laboratory. <h3>Participants</h3> Adult (8 week) and adolescent (6 week) male C57BL/6 mice. <h3>Interventions</h3> Brief oxygen exposure consisted of delivery of 100% Oxygen via hood for a total of five minutes immediately after injury; controls received room air and/or anesthesia only. <h3>Main Outcome Measures</h3> Optokinetic Response was assessed over three days. Retinal tissue was analyzed for protein/RNA expression, and serum assayed for cytokine levels. <h3>Results</h3> Although visual impairment after injury was similar between ages, oxygen more reliably improved OKR deficits in adolescents. Oxygen does not prevent retinal cell loss but does reduce pro-apoptotic markers in the retina in both groups. We anticipate a greater increase in injury-associated markers in adolescent mice compared to adults. <h3>Conclusions</h3> Even though pro-apoptotic markers in retinal cells were reduced, visual deficits persisted. Moreover, brief oxygen exposure appeared to be more beneficial for adolescent mice than for adults. Although preliminary, these results may suggest adolescent mice are more amenable to treatment for TON than adults. <h3>Author(s) Disclosures</h3> There are no conflicts to submission from any author.
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