Abstract
After the offset of illumination, barnacle photoreceptors undergo a large hyperpolarization that lasts seconds or minutes. The mechanisms that generate this afterpotential were studied by recording afterpotentials intracellularly from the medial photoreceptors of the giant barnacle B. nubilis. The afterpotential has 2 components with different time-courses: an earlier component due to an increase in conductance to K+ that is not blocked by extracellular tetraethylammonium ion (TEA+) or 3-aminopyridine (3-AP) and a later component that is sensitive to cardiac glycosides and that requires extracellular K+, suggesting that it is due to an electrogenic Na+ pump. The K+ conductance component increases in amplitude with increasing Ca2+ concentration and is inhibited by extracellular Co2+; the Co2+ inhibition can overcome by increasing the Ca2+ concentration. The K+ conductance component is Ca2+ dependent. An afterpotential similar to that evoked by a brief flash of light is generated by depolarization with current in the dark and by eliciting Ca2+ action potentials in the presence of TEA+ in the soma, axon or terminal regions of the photoreceptor. The action potential undershoot is generated by an increase in conductance to K+ that is resistant to TEA+ and 3-AP and inhibited by Co2+. The similarity in time-course and pharmacology of the hyperpolarzing afterpotentials elicited by a brief flash of light, depolarization with current and an action potential indicates that Ca2+-dependent K+ channels throughout the photoreceptor membrane are responsible for all 3 hyperpolarizing events.