The apamin-sensitive potassium current in frog skeletal muscle: its dependence on the extracellular calcium and sensitivity to calcium channel blockers

Abstract

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⁺×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.