The regulatory expression of neuronal nitric oxide synthase in the ischemic rat retina

We investigated the expression and cellular localization of neuronal nitric oxide synthase (nNOS) in the rat retina, following ischemic injury induced by transient increase of intraocular pressure. In the normal retina, nNOS immunoreactivity was localized to certain populations of amacrine cells, di splaced amacrine cells and a few bipolar cells. Following transient ischemi a, retinal neurons expressing the immunoreactivity increased and peaked thr ee days after reperfusion. Quantitative evaluation using immunoblotting con firmed that nNOS expression showed a peak value (500% of control levels) at 3 days, and then decreased again to 150% of controls by 4 weeks after repe rfusion. Our findings suggest that this overproduced NO may act as a neurot oxic agent in the ischemic rat retina. NeuroReport 12:3385-3389 (C) 2001 Li ppincott Williams & Wilkins.