[The role of nitric oxide in the ischemic retina]

Retinal ischemia induces a large increase in the release of glutamate, which exerts its toxic action by way of NMDA (N-methyl-D-aspartate) receptors onto amacrine cells and retinal ganglion cells. Glutamate released during ischemia and especially during reperfusion first stimulates non-NMDA receptors and depolarizes the retinal neurons. As the membrane potentials are depolarized more from the resting membrane potentials, the blockade of NMDA receptors induced by Mg2+ was released. Ca(2+)-influx through the NMDA receptors activates nitric oxide synthase of some amacrine cells, which produce nitric oxide (NO). NO at low concentrations inhibits the NMDA receptors and thereby prevents from retinal neuronal death. By contrast, NO at higher concentrations, interacting with oxygen radicals, becomes toxic and mediates glutamate-induced delayed retinal neuronal death.