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B. Slater, Y. Guo, S. L. Bernstein; Retinal Ganglion Cells Die After Optic Nerve Infarct by Apoptosis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4197.
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© ARVO (1962-2015); The Authors (2016-present)
In clinical cases of anterior ischemic optic neuropathy (AION), optic nerve damage results in regional retinal dysfunction and retinal ganglion cell (RGC) death. We wanted to determine the regional RGC loss distribution, mechanism and timing of RGC death, in a model of AION, rodent anterior ischemic optic neuropathy (rAION).
rAION was induced in male Wistar rats. Animals were euthanized at different times post-induction (0-30 days). We injected FITC-conjugated annexin V, which labels cells dying by apoptosis, 1 hour prior to euthanasia. Retinae were collected, fixed and examined by flat mount fluorescent analysis, to allow evaluation of regional RGC death. RGC apoptotic cell death was confirmed by retinal cross section and optic nerve crush.
Post-rAION, RGCs die by apoptosis. The peak of cell death occurs at days 10-15, but apoptotic cells are still seen past 21 days. In eyes subjected to optic nerve crush, gross RGC apoptosis was apparent at day 9. RGC death following rAION occurred regionally, with whole quadrant involvement, and sparing of other retinal regions. However, general RGC loss was seen across the entire retina as well.
rAION results in later RGC death than do traumatic optic nerve damage models, with maximal apoptosis occurring in the 2nd-3rd week post-insult. The regional retinal RGC loss suggests that a measure of retinotopic organization occurs in the rodent optic nerve similar to primates and humans. The flat mount, ex vivo apoptosis assay enabled a rapid, robust analysis of RGCs. It also suggests a extended time period exists to prevent retinal ganglion cell loss post-insult with neuroprotective therapies.
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