The apamin-sensitive potassium current in frog skeletal muscle: its dependence on the extracellular calcium and sensitivity to calcium channel blockers.
Slow outward potassium currents were recorded in isolated frog skeletal muscle fibres using the double mannitol-gap voltage-clamp technique. Detubulated fibres failed to generate a slow outward current, and apamin had no effect on the remaining current. The maximum blocking effect of organic and inorganic Ca2+-channel blockers on the slow outward channels of intact fibres was larger than that of apamin. Apamin failed to induce an additional block when applied after Ca2+-channel blockers. In a low-Ca2+ solution (OCa, EGTA 1 mM) the slow outward current was slightly increased and the blocking effect of apamin was enhanced. A Ca2+-rich solution (Ca2+ X 10) increased the slow outward current and the blocking effect of apamin was drastically reduced. It is concluded that the apamin-sensitive current which is a component of the slow outward K+ current is located in the tubular membrane. Its activation seems barely dependent on the Ca2+ influx via the slow inward Ca2+ current. Apamin-receptor binding appears to be dependent on the extracellular Ca2+ concentration. Blockade of slow outward current by Ca2+-channel blockers is likely to be the result of a direct action on the slow K+ permeability rather than a consequence of Ca2+ channel inhibition.
D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001514:Bee Venoms / Q000494:pharmacology*; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004594:Electrophysiology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008870:Microtubules / Q000502:physiology; D009132:Muscles / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000502:physiology*; D011895:Rana ridibunda
D001514:Bee Venoms; D002121:Calcium Channel Blockers; D007473:Ion Channels; D001030:Apamin; D011188:Potassium; D002118:Calcium