Abstract

Photomembrane turnover in vertebrate photoreceptors is regulated by light. Rod outer segments (ROS) shed membrane filled tips at light onset, during the coexistence of two light modulated processes: a dark priming factor and a light induction event. Transduction of these two signals is not direct but appears to involve the neural retina and diffusible paracrine molecules. I propose a model wherein three paracrines control this ROS tip shedding. Melatonin, a lipid soluble dark priming molecule, is synthesized in the dark by all photoreceptor cells, diffusing freely and separating the ROS disk membranes. A second paracrine, dopamine is released from the inner retina whenever light is absorbed by the 502 nm-cones, inhibiting melatonin synthesis. Third, a proposed trophic paracrine, "rostrophin", is released in the dark from internal horizontal cells, and stabilizes the photomembrane. Shedding occurs as rostrophin decreases in the presence melatonin; briefly at light onset or continuously in red or dim white light.

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