Nitric oxide (NO) may play an important role in regulating retinal neuronal survival. While the precise impact of NO mechanisms on retinal neurons remains to be elucidated, it has been reported that low doses of NO may have a neuroprotective effect against N-methyl-D-aspartate (NMDA)-induced retinal neurotoxicity. Dopamine has also been recognized to have neuroprotective actions. Retinal dopaminergic cells can be detected by the immunohistochemical staining of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine synthesis. We observed that NMDA dramatically decreased in TH immunostaining at the junction between the inner nuclear layer and inner plexiform layer, and that this reduction in immunostaining was attenuated by the co-injection of NOC 18, an NO donor. Thus, the current review focused on the NO-dopamine interactions in the retinal neuroprotection.
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