Visual adaptation modulates a potassium conductance in retinular cells of the crayfish

Crayfish photoreceptors exhibit a voltage-dependent potassium conductance, G(K), that is generally similar to the delayed rectifier channel described in neurons and other arthropod retinular cells. G(K) activation (i.e. the a pparent threshold, V-th) occurs near the resting potential and G(K) is subs tantially reduced by 25 mM extracellular tetraethylammonium (TEA) and by in tracellular Cs+ injections, Light exposure, sufficient to reduce visual sen sitivity 100-fold, increases V-th (shifts it in the depolarizing direction) by about 20 mV. The light-dependent change in V-th does not depend upon th e corresponding increase (depolarization) of the steady-state membrane pote ntial nor does it depend upon inward calcium currents. V-th is slightly inf luenced by fluctuations in K-o associated with the light-elicited currents. During light exposure K-o (measured with K+-sensitive electrodes) increase s by 2.1 mM (equivalent to an 8 mV increase in E-K). This increase in En ma kes only a modest contribution to the light-dependent change in V-th as det ermined by perfusion with high potassium salines. Intracellular calcium inj ections increase V-th by 10 to 20 mV and reduce visual sensitivity by 5- to 10-fold. The results imply that during exposure to high levels of illumina tion K+ currents at the steady-state membrane potential are diminished by a calcium-dependent change in G(K) gating and, to a smaller degree, by a red uced K+ concentration gradient. It is notable that Ca2+ appears to inhibit both G(K) and the light-elicited conductance from both inside and outside t he plasma membrane. As a consequence of the light-dependent change in V-th. G(K) makes only modest contributions to the changes in sensitivity and spe ed normally associated with light adaption. These functions are regulated b y the transduction pathway and are revealed at the resting potential in the time course and magnitude of the light-elicited currents.