Deficits in visually guided behavior, particularly the optomotor response, are found to follow treatment of the chicken retina with a range of toxic agonists of glutamate and aspartate receptors. These agonists include kainic acid, quisquaUc acid, homocysteic acid and N-methyl D-aspartatic acid, given either alone or in combination with chemicals which antagonise some aspects of their neurotoxic actions and so cause cell loss ofvarious degress ofspecificity. Glutamate itself, when given at a high dose, causes non-specific lesions of the retina but has less effect on the optomotor response than kainate, which causes loss of a specific class of cells. Using these retinotoxins as tools of varying specificity, it is deduced that loss of the optomotor response, together with other visual impairments, is due to loss of amacrine cells and/or displaced ganghon cells. The paper includes discussion of the cellular and neurochemical organisation of the retina, retinal projections involved in the optokinetic response, as well as a summary of the modes of action of the toxins used.