The calcium current and the activation of a slow potassium conductance in voltage-clamped mouse neuroblastoma 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.