To test the hypothesis that myeloid body (MB) formation results from the shedding of retinal photoreceptor outer segments and the consequent degradation of lipids derived from outer segment disk membranes, the effect of massive outer segment shedding and the disruption of such outer segment shedding on MB formation were examined in the leopard frog. Light entrained frogs were first placed in constant light (700 lux) for 48 hours to inhibit shedding, followed by a 1.5 hours dark priming eitherin vivoorin vitro, and then returned to light for an additional 4 hours which results in massive outer segment shedding. To serve as a control, the effect of shedding disruption on MB formation was assessedin vivousing light manipulation to inhibit shedding, or mechanical removal of the neurosensory retinain vitro.The results indicate that although the phagosome numbers were clearly elevated in the samples taken from eitherin vivoorin vitroeye-cup preparations where outer segment shedding had been stimulated, there was no significant concomitant increase in Mbs number over controls kept under constant light for 48 hr or constant light 48 hr plus 1.5 hr in dark, where MBs represent approximately 5% of the total RPE cell area. In contrast, when shedding was interrupted either by removal of the neural retina immediately afterin vitroeye-cups were returned to light or by maintaining frogs in dark without light stimulation, the RPE cells contained very few phagosome, yet in both conditions RPE cells showed a two-fold increase in MB area over the shedding-stimulated controls (p=0.0001). In conclusion, MB formation appears not to be simply a direct result of photoreceptor outer segment disk shedding and membrane degradation since the interruption of photoreceptor outer segment shedding results in an increase in MB occurrence in the RPE. Based on this new evidence we now speculate that MBs in the frog RPE may be actively involved in lipid recycling related to photoreceptor outer segment membrane turnover.