Silent calcium channels generate excessive tail currents and facilitation of calcium currents in rat skeletal myoballs.

Whole-cell patch-clamp recording were employed to study facilitation of Ca2+ currents and excessive Ca2+ tail currents evoked by strong and long-lasting conditioning depolarizations in skeletal myoballs cultured from newborn rats. 2. Paired-pulse facilitation and excessive tail currents showed the same voltage dependence, becoming prominent at conditioning potentials above +30 mV. 3. Recruitment of excessive tail currents and facilitation occurred with the same time dependence (time constant (tau), approximately 200 ms to approximately 1 s), accelerating with the depolarization strength of conditioning pulses. 4. Reversal of Ca2+ current facilitation during the repolarization period between conditioning and test pulses was time- and voltage dependent. The time window of recruitment of facilitated Ca2+ currents narrowed considerably at more negative repolarization potentials (tau: approximately 10 ms at -100 mV, but approximately 1.5 at 0 mV). 5. Neither omission of internal ATP nor perfusion of the cells with the peptide inhibitor of protein kinase A (PKI) had significant effects on Ca2+ current facilitation, although internal perfusion with ATP gamma S slowly suppressed the facilitation currents by about 30%. External application of either ryanodine or caffeine under control conditions selectively and significantly suppressed the facilitated Ca2+ currents by about 30-40%. 6. We propose that facilitation of Ca2+ currents and excessive tail currents are consequences of a common mechanism linked to ryanodine receptors.