The pearl mutant mouse is hypopigmented and exhibits a significantly elevated dark-adapted (DA) threshold in comparison to the congenic wild-type mouse. The primary cause of the elevated DA threshold is not known. The subcellular immunolocalization of arrestin/S-antigen reflects the state of adaptation of rod photoreceptors. In this study, quantitative immunoelectron microscopy was used to examine the subcellular distribution of arrestin in wild-type and pearl rods as a function of light exposure. The goal was to determine whether arrestin distribution within rods of pearl and wild-type mice responds to background luminance in a comparable manner. The level of arrestin immunolabeling in DA (unilluminated) rods of pearl retinas was indistinguishable from that measured in wild-type rods. By contrast, arrestin immunolabeling in light-adapted (LA) pearl rod outer segments (ROS) was significantly greater than in wild-type LA ROS. Relative to DA ROS, arrestin labeling density increased 1.6 fold in wild-type ROS following light adaptation, as compared to a 4 fold increase in pearl ROS. These data suggest that although arrestin levels in DA pearl rods are indistinguishable from that of DA wild-type rods, net changes in arrestin immunolocalization inresponse to light exposurereflect the effects of the pearl mutation at the level of the rod outer segment. The possible implication of this finding is discussed in view of the proposed role of arrestin in the down-regulation of the enzymatic cascade of phototransduction.