Brief, intracellularly injected pulses of cyclic GMP transiently depolarized 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 cyclic GMP 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 cyclic GMP 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. This similarity suggests that the initial phase of the receptor potential is controlled by light-activated PDE. Both EGTA and saturating doses of cyclic GMP block the light response, but only cyclic GMP increases response latency, which suggests that if calcium is involved in transduction, it is controlled by the hydrolysis of cyclic GMP. After brief pulses of cyclic AMP, a new steady state of increased depolarization occasionally develops. The effects described above also occur under these conditions. The results are consistent with the hypothesis that light-activated hydrolysis of cGMP is an intermediary process in transduction.

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