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M-H Chun, JS Gwon, WK Ju, SJ Oh, JI Moon; The Regulatory Expression of Neuronal Nitric Oxide Synthase in the Ischemic Rat Retina and the Effect of NO on the Retinal Neurons of the Rat . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1997.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To investigate the expression and cellular localization of neuronal nitric oxide synthase (nNOS) in the rat retina following transient ischemia and the effect of NO on apoptosis in rat retinal neurons. Methods: The intraocular pressure was raised to 120 mmHg for 60 min. Immunocytochemistry and immunoblotting using anti-nNOS antisera, TUNEL techniques, and electron microscopy were performed. Results: In the normal retina, nNOS immunoreactivity was localized to certain populations of amacrine cells, displaced amacrine cells and a few bipolar cells. Following transient ischemia, retinal neurons expressing the immunoreactivity increased and peaked three days after reperfusion. Quantitative evaluation using immunoblotting confirmed that nNOS expression showed a peak value (500% of control levels) at three days, and then decreased again to 150% of controls by four weeks after reperfusion. In the sodium nitroprusside (SNP), a NO donor, -treated retina, TUNEL-positive cells were observed in the outer nuclear layer (ONL), but not in the inner retina. Inner retinal neurons died by necrosis. No photoreceptor cells were found in the ONL after seven days. Immunoblotting confirmed that neuronal NO synthase expression increased up to five days (c. 170% of control levels), and then declined by seven days. Conclusion: Retinal neurons in the inner retina respond to ischemic injury by the increased production of nNOS. The overproduced NO acts as a neurotoxin to retinal neurons, which in turn over-release glutamate during their degeneration. The over-released glutamate induces upregulation of nNOS production in the inner retinal neurons.
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