The effects of low calcium and background light on the sensitivity of toad rods

Abstract
The effects of decreases in extracellular Ca2+ concentration on the intracellularly recorded light responses of rods from the toad, B. marinus. In agreement with previous results (Brown Pinto, 1974; Lipton, et al., 1977), Ca2+ concentrations < 10-6 M produced a depolarization of rod resting membrane potential of .apprx. 30-40 mV and a corresponding increase in the maximum amplitude of the rod''s light responses, so that saturating flashes in normal and low Ca2+ Ringer produced hyperpolarizations to approximately the same membrane potential. Rod sensitivity was reduced in low Ca2+ Ringer by an amount dependent on the extracellular Ca2+, [Ca2+]0 concentration. At 10-6 M-Ca2+, sensitivity was 0.6 log units below normal. It dropped nearly linearly with [Ca2+]0 to a value .apprx. 4.0 log units below normal at 10-9 M Ca2+. Most of the decline occurred within 1-2 min after the solution change as the membrane potential depolarized, but sensitivity continued to fall slowly with time at the lowest Ca2+ concentrations. Exposure to low Ca2+ solutions altered the kinetics of the receptor response to brief flashes, delaying response onset and time-to-peak but affecting the time course of decay very little. The sensitivity of the rod to maintained steps of light was also reduced in low Ca2+. The changes in sensitivity produced by background illumination were very much smaller in low Ca2+ than in normal Ringer. In some cases backgrounds actually increased sensitivity. In 10-8 M-Ca2+, backgrounds which themselves produced no response in the rod and no changes in rod sensitivity produced large decreases in response latency for responses of all amplitudes, and pronounced changes in time-to-peak and time-to-decay for moderate and large amplitude responses. Since the effects of background light and low Ca2+ on the wave form of the rod are distinct and in some cases antagonistic, and since the changes in receptor sensitivity produced by backgrounds and low Ca2+ are not additive, the decreases in sensitivity produced by exposure to low Ca2+ appear to be caused by a mechanism distinct from normal light adaptation. Apparently, they are caused by an increase in the buffering capacity of the receptor cytosol for Ca2+, and Ca2+ may be the excitatory messenger or internal transmitter, as originally suggested by Yoshikami et Hagins (1971).