Glutamate is the major excitatory neurotransmitter in the rat visual system. Using quantitative autoradiography the effect of unilateral orbital enucleation on [3H]kainate, [3H]alpha-amino-3-hydroxy-5-methyl- isoxazole-4-propionic acid [( 3H]AMPA) and [3H]glutamate binding to kainate, quisqualate and NMDA receptors respectively has been examined within anatomical components of the visual pathway at 4 time points up to 20 days post-lesion. The time course for the degeneration of retinal projection fibres was assessed in a separate group of animals by quantifying [3H]cyclohexyladenosine [( 3H]CHA) binding to presynaptic adenosine A1 receptors. Over the first 5 days after orbital enucleation, there were no significant alterations in glutamate or adenosine A1 receptor binding in visual structures of the visually deprived hemisphere. However, at 10 days post-lesion [3H]AMPA binding was significantly reduced (30%) in the visually deprived superior colliculus but unaltered in other visual structures. At this time point there was also a significant reduction (50%) in [3H]CHA binding in the visually deprived superior colliculus but not in other retino-recipient nuclei. There were similar changes in [3H]AMPA and [3H]CHA binding at 20 days post-enucleation. [3H]Kainate binding was significantly increased in the visually deprived superior colliculus only at 20 days post-enucleation. Saturation analysis of [3H]kainate and [3H]AMPA binding at this time point indicated a selective increase in the Bmax value for the high affinity [3H]kainate binding site and a concomitant decrease in the Bmax value for the high affinity [3H]AMPA binding site in the visually deprived superior colliculus. There were, however, no significant alterations in [3H]AMPA or [3H]kainate binding in other primary projection areas or in secondary visual areas (e.g. visual cortex) at any time point. NMDA sensitive [3H]glutamate binding was unaltered in the visually deprived hemisphere up to 20 days post-enucleation. These results suggest an upregulation of kainate receptors in the visually deprived superior colliculus after orbital enucleation and a loss of presynaptic quisqualate receptors on degenerating retinal fibres. The plastic alterations in kainate receptors in the superior colliculus are supportive of electrophysiological data suggesting a physiological role for these sites in mediating excitatory postsynaptic potentials in tectal neurons.