Physiological evidence that light-mediated decrease in cyclic GMP is an intermediary process in retinal rod transduction.

Abstract

Brief, intracellularly injected pulses of cGMP transiently depolarize toad retinal rod outer segments (ROS). The depolarization is antagonized by light, perhaps by the activation of phosphodiesterase (PDE), as shown in the biochemical studies of others. As measured by the antagonism of cGMP pulses by light, PDE activity peaks after the peak of the receptor potential and has approximately the same recovery time as the membrane voltage after weak illumination, but recovers more slowly than the membrane potential after strong illumination, as sensitivity does in other preparations. A cGMP pulse delivered just after the hyperpolarizing phase of the receptor potential tends to turn off the light response. The kinetics of recovery from this turnoff are similar to those of the initial phase of the receptor potential. The initial phase of the receptor potential may be controlled by light-activated PDE. Both EGTA [ethylene glycol-bis(.beta.-amino ethyl ether)-tetraacetic acid] and saturating doses of cGMP block the light response, but only cGMP increases response latency, which suggests that if Ca is involved in transduction, it is controlled by the hydrolysis of cGMP. After brief pulses of cGMP, a new steady state of increased depolarization occasionally develops. These effects occur under these conditions. Apparently, light-activated hydrolysis of cGMP is an intermediary process in transduction.