Abstract
Rod photoreceptor outer segment material production was autoradiographically monitored in the right eye of rats two log units vitamin A-deficient as determined by extinguishing the B wave of the electroretinogram. Each rat was then given vitamin A and two weeks later the study was repeated in the left eye. Control animals were also monitored. A 10-day interval was required for complete renewal of the rod outer segment material in deficient, postdeficient, and normal eyes. Each deficient animal showed an increase in thickness of its layer of rods after receiving vitamin A. These findings indicate that the rate of rod outer segment material production is decreased at low levels of vitamin A deficiency. The density of radioactive labeling increased progressively from deficient to post-deficient to control animals. The decrease in density of labeling in the post-deficient animals when compared to the normal control animal suggests that vitamin A deficiency can be used for "rod thinning" to permanently decrease the quantity of rod outer segment material produced. This could be of therapeutic benefit in conditions where a relative breakdown exists in the normal equilibrium between production of rod outer segment material and its removal by the pigment epithelium of the retina.