Extended vitamin A deficiency in the cat led to an abnormal appearance in the tapetal fundus with the formation of a dark brown streak centered on the area centralis. At this time rod sensitivity, as measured by the b-wave of the electroretinogram, was reduced by more than two log units; the level of rod visual pigment was reduced by about 90% throughout the paracentral retinal region and was essentially absent from the area centralis. Following oral supplementation with vitamin A there was a rapid partial recovery of both rhodopsin levels and rod sensitivity. Further recovery continued over more than 18 days to levels that were not substantially below normal. This recovery was absent from the area centralis, in which measured visual pigment levels remained very low. In supplemented cats, the brown color in the fundus faded but there remained a small hyper-reflective zone at the area centralis. Morphological examination of the central retina in a supplemented cat showed an outer nuclear layer reduced to one or two rows in the small zone with low rhodopsin levels. Cone but not rod photoreceptors were present in this zone and they appeared to lack outer segments. During recovery, the increase in rod sensitivity was approximately linearly related to the recovery of rhodopsin levels. Thus, in these conditions reduction in sensitivity resulting from previous vitamin A deficiency was limited by the ability of the photoreceptors to absorb incident quanta. The time course of the recovery of rhodopsin and sensitivity suggests that at least two processes were involved. The faster of these may be the regeneration of rhodopsin from existing opsin molecules in the outer segments, while the slower may depend on the renewal of the outer segments themselves.