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Y. Guo, S. L. Bernstein; Inducible Nitric Oxide Synthase Expression in Rodent Model of Non-Arteritic Anterior Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1080.
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Non-arteritic anterior optic neuropathy (NAION) is associated with optic edema. Nitric oxide (NO) metabolism and NO expression have been postulated to be involved in vascular deregulation and tissue edema following ischemia. We wanted to use the rodent model of non-arteritic anterior ischemic optic neuropathy (rAION) to evaluate changes in inducible nitric oxide synthase (iNOS) and NO-induced nitrotyrosine activity in the optic nerve (ON) following sudden ON ischemia.
Male Sprague-Dawley rats (120-150g) were utilized in this study. rAION was induced as previously described in one eye. The other eye was left as an untreated control. Following induction, animals were allowed to recover, and then euthanized at either 4 hours or 1 day post-induction. Globes and ONs were enucleated and fixed in 2% PFA overnight, then transferred to 30% sucrose for frozen section preparation. Immunohistochemistry was carried out using antibodies to iNOS and nitrotyrosine antibodies at 1:2000, and 1:1000 respectively. Results were evaluated using confocal microscopy. Quantitative iNOS mRNA gene expression was also evaluated using total RNA from optic nerve head at identical time points.
There was elevated iNOS mRNA and protein expression in the optic nerve head and proximal portion of the optic nerve at 4 hours post rAION induction. iNOS protein expression was transient and decreased in the ON by 1 day. Nitrotyrosine expression was not elevated at 4 hours, but changed thereafter, compared with control eyes, proximal to and at the stroke site.
Following ON stroke, there is rapid elevation of iNOS at the optic nerve head, with decline by 1 day post rAION induction. This suggests that while iNOS activation is associated with early vascular ischemia, and may be involved with development of early ON edema, continued iNOS activity does not play a major role in maintaining ON edema in the later stages of the disorder.
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