ACTIVATION OF A SLOW OUTWARD CURRENT BY THE CALCIUM RELEASED DURING CONTRACTION OF CULTURED RAT SKELETAL-MUSCLE CELLS

A slow outward current, activated during depolarization, which induced contraction in whole-cell patch-clamped rat skeletal muscle cells in primary culture [10], was extensively characterized in the present stu dy. This current, I(O), was simultaneously recorded with the contracti on as a slow outward current during the test pulse, and a slow outward bell-shaped tail after repolarization. I(O) never appeared below the threshold potential for contraction, and the tail amplitude displayed a similar evolution with peak contraction amplitude as a function of m embrane potential. This feature is consistent with the fact that I(O) was suppressed when contraction was blocked by 5 muM nifedipine [10], and it suggests that I(O) was dependent on calcium released during con traction. This was confirmed by the fact that the presence of 10 mM EG TA in the patch pipette prevented the development of both contraction and I(O), and that I(O) could be activated during caffeine-induced con tractures without applying depolarizations. I(O) could be carried by K + or Cs+ ions, but not by Na+. The pharmacology of I(O) was different from that of Ca2+-dependent BK and SK channels, since it was resistant to tetraethylammonium (135 mM), charybdotoxin (25 nM) and apamin (50 nM). I(O) was also insensitive to 4-aminopyridine (1 mM) but blocked b y 5 mM Ba2+ without change to contraction. It was concluded that rat c ultured myoballs exhibit a Cs+ permeation through an atypical K+ chann el type, which is activated by the calcium released during contraction .