Abstract
The membrane potential of rods in the isolated toad retina was recorded while changing the ionic composition of the extracellular medium. Cs+ at a concentration of 1 mM was sufficient to completely block the sag from the peak to the plateau in the bright-flash voltage response. In the presence of 10 mM-Cs+ the bright-flash response increased in amplitude to about 90 mV, thus reaching an absolute membrane potential of between -110 and -135 mV. These responses consisted of an initial fast component of about 35 mV followed by a much slower component which could be as large as 50 mV. At the peak of the initial fast component the rod membrane conformed closely to the behavior of a K+ electrode with a P[permeability]Na/PK ratio of 0.023. On average the amplitude of the slow component was about 35 mV in the presence of 2.6 mM-K+ and was reduced to about 25 mV in a K+-free Ringer. Addition of 100 .mu.M-strophanthidin to the perfusate induced several reversible changes in the electrical activity of rods. The dark resting membrane potential depolarized by about 5 mV and the kinetics of the voltage response to dim flashes of light slowed down. The voltage sensitivity initially increased by about 30%, but the peak of the response to a bright flash of light was reduced by about 13 mV. In rods treated with 10 mM-Cs+ the slow component present in the bright flash response was abolished by strophanthidin with an apparent Km of 3 .mu.M. The amplitude of the slow component decreased with a time lag of about 2 min when external Na+ was reduced. A previous exposure of the retina to a Na+-free Ringer solution for at least 3 min modified the voltage photoresponse in a way similar to that observed in the presence of 100 .mu.M-strophanthidin. When external Ca2+ concentration ([Ca2+]o) was increased from 2 to 5 mM the slow component decreased by about 30%. When [Ca2+]o was reduced the slow component increased. A 2-fold increase was observed when [Ca2+]o was lower than 10-4 M. The slow component of the voltage response in the presence of external Cs+ apparently is caused by an electrogenic current driven by the Na+-K+ transport system, during a voltage-dependent block of external Cs+ of some K+ channels.