Cyclic GMP injected into retinal rod outer segments increases latency and amplitude of response to illumination.

We have injected cyclic GMP intracellularly by iontophoresis through the recording electrode into single rod outer segments of the isolated superfused retina of the toad. Bufo marinus. The two most marked effects of the injection are: (i) the latency of the hyperpolarizing membrane-potential change caused by illumination is increased from 5 to 50 times normal, the increase in latency being inversely proportional to the light stimulus intensity; and (ii) the amplitude of the hyperpolarizing receptor potential is increased. These effects are reversible. Our findings are consistent with the hypothesis that cyclic GMP is a link in the molecular chain of events that controls the inward flow of sodium ions in light and darkness. The increased latency we observe after injection of cyclic GMP may be caused by a time delay necessary for light-activated phosphodiesterase to hydrolyze the excess cyclic GMP. By this reasoning the excess cyclic GMP perpetuates the dark current long after illumination. Excitation may be controlled by cyclic GMP if, as our experiments suggest, its hydrolysis initiates the hyperpolarizing receptor potential.