| First Author | Fleig A | Year | 1996 |
| Journal | J Physiol | Volume | 496 ( Pt 2) |
| Pages | 339-45 | PubMed ID | 8910220 |
| Mgi Jnum | J:38579 | Mgi Id | MGI:85959 |
| Doi | 10.1113/jphysiol.1996.sp021689 | Citation | Fleig A, et al. (1996) Absence of Ca2+ current facilitation in skeletal muscle of transgenic mice lacking the type 1 ryanodine receptor. J Physiol 496(Pt 2):339-45 |
| abstractText | 1. Whole-cell patch-clamp recordings were used to study voltage-dependent facilitation of Ca2+ currents and excessive Ca2+ tail current in skeletal myoballs cultured from wild-type and transgenic mice expressing a null mutation of the ryanodine receptor (RyR) type 1 (dyspedic myoballs). 2. Ca2+ current density in dyspedic myoballs was reduced by about 60% compared with wild-type cells, with dihydropyridine-binding capacity largely retained. 3. Strong and long-lasting depolarizations (+80 mV and 600 ms), which normally produce excessive tail currents upon repolarization in control cells, failed to do so in dyspedic myoballs. 4. Dyspedic myoballs also failed to produce both Ca2+ current facilitation and the left shift of the current-voltage (I-V) curve induced by paired-pulse stimulation. 5. We propose that excessive tail currents and facilitation arise from silent Ca2+ channels acting as the voltage sensors in excitation-contraction coupling. |
