In male hooded rats, depletion of norepinephrine and dopamine by a-methyl-paratyrosine (AMT) significantly increased the latencies of early peaks in flash-evoked potentials recorded from the visual cortex, lateral geniculate nucleus, and optic tract. These effects were not produced by depletion of norepinephrine by FLA-63, blockade of muscarinic acetylcholine receptors by scopolamine, or blockade of opiate receptors by naloxone. AMT effects occurred only when flashes were used; optic tract stimulation failed to reveal the drug-induced changes. In a dose-response study, haloperidol produced effects similar to those of AMT. L-Dopa + R04-4602 reversed some of the effects of AMT. It is concluded that depletion of retinal dopamine impairs the timing of retinal responses to light.