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Affiliation
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Department of Ophthalmology and Visual Sciences, Vanderbilt University, 2213 Garland Ave, 11425 MRB IV, Nashville, TN, 37232, United States tonia.rex@Vanderbilt.edu. |
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Abstract
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PURPOSE. To characterize retinal changes and assess vision after an eye-directed air blast.
METHODS. Adult C57Bl/6 mice were exposed to a blast directed at one eye. Optical coherence tomography and histology were performed to assess retina and optic nerve integrity. Cell death, oxidative stress and glial reactivity were examined by immunohistochemistry. Visual changes were measured by electroretinogram recordings and the optokinetic reflex.
RESULTS. In the outer retina, eye blast caused retinal pigment epithelium vacuoles and rare retinal detachments followed by regional cell death. Labeling for nitrotyrosine and markers of pyroptosis (caspase-1) and necroptosis (RIP-1, 3) increased, primarily in the inner retina, after blast. Caspase-1 labeling was restricted primarily to the starburst amacrine cells. A few degenerating axons were detected at 28 days post-blast. Despite a lack of substantial cell death or decreased electroretinogram, there was a deficit in visual acuity after blast.
CONCLUSIONS. Oxidative stress, neuroinflammation, and cell death became increasingly prevalent over time post-blast suggestive of an ongoing neurodegenerative response. Outer retinal changes either resolved or remained focal. In contrast, inner retinal changes were more robust and spread from focal regions to the entire retina over time post-blast. Our model of eye blast trauma causes molecular changes and a decrease in visual acuity within the first month post-blast despite a lack of overt eye injury. This subtle response matches the delayed presentation of visual deficits in some blast-exposed Veterans.
Language: en |