Excessive repolarization‐dependent calcium currents induced by strong depolarizations in rat skeletal myoballs.

1. Whole‐cell patch‐clamp recordings were used to study voltage‐dependent Ca2+ currents in skeletal myoballs cultured from newborn rats. 2. Depolarizing voltage pulses evoked classical L‐type Ca2+ currents, whereas repolarization induced tail currents, whose properties deviated from the expected behaviour of the preceding Ca2+ currents in both voltage dependence and kinetics. 3. Depolarizations of up to +10 mV primarily recruited tail currents that correspond to the Ca2+ channels activated and conducting during the depolarizing pulse, but stronger depolarizations yielded an additional tail current component that exceeded the ‘normal’ tail current amplitude by several‐fold. 4. Activation kinetics of the tail currents were biexponential, with a fast time constant matching the activation time course of the pulse currents (tau approximately 40 ms) and an additional slower component with a voltage‐dependent time course that had no kinetic counterpart in the pulse currents (tau approximately 150‐600 ms). 5. Both pulse and tail currents were blocked by the dihydropyridine, PN200‐110, suggesting that they represent Ca2+ channels of the L‐type. 6. We suggest the presence of at least two subsets of dihydropyridine‐sensitive Ca2+ channels in skeletal muscle cells. One subset has classical L‐type channel characteristics and the other has anomalous gating behaviour that is ‘activated’ or ‘primed’ by strong and long‐lasting depolarizations without conducting significant Ca2+ current‐‐however, upon repolarization, this subset of channels generates large tail currents.