SILENT CALCIUM CHANNELS GENERATE EXCESSIVE TAIL CURRENTS AND FACILITATION OF CALCIUM CURRENTS IN RAT SKELETAL MYOBALLS

Authors
Citation
A. Fleig et R. Penner, SILENT CALCIUM CHANNELS GENERATE EXCESSIVE TAIL CURRENTS AND FACILITATION OF CALCIUM CURRENTS IN RAT SKELETAL MYOBALLS, Journal of physiology, 494(1), 1996, pp. 141-153
Citations number
20
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
494
Issue
1
Year of publication
1996
Pages
141 - 153
Database
ISI
SICI code
0022-3751(1996)494:1<141:SCCGET>2.0.ZU;2-3
Abstract
1. Whole-cell patch-clamp recordings were employed to study facilitati on of Ca2+ currents and excessive Ca2+ tail currents evoked by strong and long-lasting conditioning depolarizations in skeletal myoballs cul tured from newborn rats.2. Paired-pulse facilitation and excessive tai l currents showed tile 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 (tim e constant (tau), similar to 200 ms to similar to 1 s) accelerating wi th tie depolarization strength of conditioning pulses. 4. Reversal of Ca2+ current facilitation during the repolarization period between con ditioning and test pulses was time- and voltage dependent. The time wi ndow of recruitment of facilitated Ca2+ currents narrowed considerably at more negative repolarization potentials (tau: similar to 10 ms at -100 mV, but similar to 1.5 s at 0 mV). 5. Neither omission of interna l 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 fac ilitation currents by about 30%. External application of either ryanod ine or caffeine under control conditions selectively and significantly suppressed the facilitated Ca2+ currents by about 30-40 %. 6. We prop ose that facilitation of Ca2+ currents and excessive tail currents are consequences of a common mechanism linked to ryanodine receptors.