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Richard J. Blanch, Zubair Ahmed, Attila Sik, David R. J. Snead, Peter A. Good, Jenna O'Neill, Martin Berry, Robert A. H. Scott, Ann Logan; Neuroretinal Cell Death in a Murine Model of Closed Globe Injury: Pathological and Functional Characterization. Invest. Ophthalmol. Vis. Sci. 2012;53(11):7220-7226. doi: https://doi.org/10.1167/iovs.12-9887.
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© ARVO (1962-2015); The Authors (2016-present)
Blunt ocular trauma causes severe retinal injury with death of neuroretinal tissue, scarring, and permanent visual loss. The mechanisms of cell death are not known, and there are no therapeutic interventions that improve visual outcome. We aimed to study the extent, distribution, and functional consequences of cell death by developing and characterizing a rat model of retinal injury caused by blunt ocular trauma.
The eyes of anesthetized adult rats were injured by either weight drop or low-velocity ballistic trauma and assessed by clinical examination, electroretinography, light microscopy, electron microscopy, and TUNEL. Projectile velocity was measured and standardized.
Weight drop did not cause reproducible retinal injury, and the energy threshold for retinal injury was similar to that for rupture. Low-velocity ballistic trauma to the inferior sclera created a reproducible retinal injury, with central sclopetaria retinae, retinal necrosis, and surrounding commotio retinae with specific photoreceptor cell death and sparing of cells in the other retinal layers. The extent of photoreceptor cell death declined and necrosis progressed to apoptosis with increasing distance from the impact site.
This is the only murine model of closed globe injury and the only model of retinal trauma with specific photoreceptor cell death. The clinical appearance mirrors that in severe retinal injury after blunt ocular trauma in humans, and the ultrastructural features are consistent with human and animal studies of commotio retinae. After ocular trauma, photoreceptor apoptosis may be prevented and visual outcomes improved by blocking of the cell death pathways.
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