EXCESSIVE REPOLARIZATION-DEPENDENT CALCIUM CURRENTS INDUCED BY STRONGDEPOLARIZATIONS IN RAT SKELETAL MYOBALLS

1. Whole-cell patch-clamp recordings were used to study voltage-depend ent Ca2+ currents in skeletal myoballs cultured from newborn rats. 2. Depolarizing voltage pulses evoked classical L-type Ca2+ currents, whe reas repolarization induced tail currents, whose properties deviated f rom the expected behaviour of the preceding Ca2+ currents in both volt age dependence and kinetics. 3. Depolarizations of up to +10 mV primar ily recruited tail currents that correspond to the Ca2+ channels activ ated and conducting during the depolarizing pulse, but stronger depola rizations yielded an additional tail current component that exceeded t he 'normal' tail current amplitude by several-fold. 4. Activation kine tics of the tail currents were biexponential, with a fast time constan t matching the activation time course of the pulse currents (tau appro ximate to 40 ms) and an additional slower component with a voltage-dep endent time course that had no kinetic counterpart in the pulse curren ts (tau approximate to 150-600 ms). 5. Both pulse and tail currents we re blocked by the dihydropyridine, PN200-110, suggesting that they rep resent Ca2+ channels of the L-type. 6. We suggest the presence of at l east two subsets of dihydropyridine-sensitive Ca2+ channels in skeleta l muscle cells. One subset has classical L-type channel characteristic s 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.