Figure 6. Model for visual cycle function. The different distributions reported in this study led to a model for visual cycle function. all-trans-Retinol, released from rod photoreceptor cells during illumination, is taken up via the apical surface of RPE cells. In turn, 11-cis-retinal is released from the apical surface for regeneration of rhodopsin. Visual cycle enzymes convert all-trans-retinol to 11-cis-retinal within the cell body. The presence of CRALBP and CRBP in both the cell body and apical processes allows these retinoid-binding proteins to facilitate diffusion of 11-cis-retinal and all-trans-retinol from sites of release and uptake, respectively, in the apical processes to and from enzymatic processing in the cell body. Within the apical processes, NHERF1, ezrin, and actin interact with CRALBP. Release of 11-cis-retinal occurs by an unknown mechanism but may be related to complex formation of interaction of CRALBP, ezrin, and EBP50/NHERF1 in the apical processes. Release and uptake of retinoids occurs along the whole apical membrane. It is depicted only from the apical processes for clarity. CRALBP and CRBP facilitate diffusion by providing binding sites for retinoids, whose diffusions are driven in either scleral or vitreal directions by concentration gradients generated by esterification of retinol by LRAT and perhaps affinity of opsin for 11-cis-retinal, respectively.