Abstract
1. Endogenous zinc is localized mainly in the retinal photoreceptors and retinal pigment epithelial cells in the mammalian retina. No other types of retinal neurons contain large amounts of zinc. 2. Low concentrations of exogenous zinc, like the N-methyl- D-aspartate (NMDA) antagonist MK-801, counteract the NMDA-induced changes in the γ-aminobutyric acid (GABA) immunoreactivity in the rabbit retina. However, greater concentrations of zinc exacerbate the effects of NMDA and ischemic-like insults (lack of glucose and oxygen) on GABA immunoreactivity. The data suggest that low concentrations of zinc are neuroprotective, but higher concentrations of zinc have a negative effect. 3. When low concentrations of zinc are present during ischemic-like insults to the retina, the GABA immunoreactivity is localized to the Müller cells, suggesting that the metabolism of GABA in the Müller glial cells is prevented. 4. Ascorbate/iron-induced generation of reactive oxygen species (ROS) in the retina is prevented by deferoxamine but not by zinc. High concentrations of zinc potentiate the ascorbate/iron induced formation of ROS.
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