CALCIUM CURRENT AND THE ACTIVATION OF A SLOW POTASSIUM CONDUCTANCE IN VOLTAGE-CLAMPED MOUSE NEURO-BLASTOMA CELLS

1. The Ca2+ inward current (ICa) and a slow outward current in differentiated cells of mouse neuroblastoma clone N1E‐115 have been studied under voltage‐clamp conditions. 2. ICa shows voltage‐ and time‐dependent inactivation when evoked by step‐wise depolarizations in Na+‐free solution containing high [Ca2+] (20 nM) and tetraethylammonium (TEA, 25 mM). Ba2+ and Sr2+ can substitute for Ca2+. 3. Holding potentials below ‐70 mV maximal activate ICa. Half inactivation occurs at ‐56 mV and ICa is completely inactivated beyond holding levels of ‐30 mV. Maximum peak currents are of the order of 10(‐4) A/cm2 and the reversal potential ranges from +40 to +60 mV. The ICa inactivation time course follows first‐order kinetics with a voltage‐depedent time constant ranging from 25 to 100 msec. 4. The striking resemblance between ICa and the Ca2+ current in the unfertilized mouse oocyte (Okamoto, Takahashi & Yamashita, 1977) is discussed. 5. A slow outward current with a rise time of several seconds is recorded on voltage steps beyond ‐20 mV in high [Ca2+] solutions. It is carried primarily by K+ on account of the value of the reversal potential and its dependence on [K]0. This K+ current is TEA‐insensitive and is blocked by Ca2+ antagonists. 6. The slow K+ current (IK(Ca)) is suggested to be mediated by Ca2+ influx, but the voltage‐dependence of the underlying conductance (GK(Ca)) differs significantly from the ICa voltage‐dependence. 7. The results are consistent with the hypothesis that IK(Ca) depends both on ICa and on membrane potential. An alternative hypothesis is briefly discussed. © 1979 The Physiological Society