Resting potential of the mouse neuroblastoma cells: I. The presence of K + channels activated at high K + concentration but closed at low K + concentration including the physiological concentration

Abstract

The effects of changes in extracellular K + concentration ([K +] o) on the resting membrane potential, the input resistance and 86Rb efflux (as a marker of K + efflux) were examined with use of the cultured mouse neuroblastoma cells (N-18 clone). The results obtained are as follows. (1) The membrane potential was depolarized, with an increase in [K +] o at concentrations above 10–20 mM at a rate of 55–58 mV per 10-fold change in [K +] o, but practically unchanged with varying [K +] o below this concentration. (2) Above the critical [K +] o of 10–20 mM, the input membrane resistance decreased sharply by a factor of 1 4 − 1 5 with an increase in [K +] o. A similar decrease in the resistance occurred even under the conditions that the membrane potential was held at control level (about −55 mV) by a steady-state current passage. (3) Elimination of Na + and Cl − from the external solution brought about practically no change in the membrane potential. (4) A fractional escape rate of 86Rb from N-18 cells remained constant at relatively low level (0.125%/min on average) in the low [K +] o range, but increased sharply with increasing [K +] o above 15 mM (e.g., approx. 3.4- and 4.5-fold at 30 and 100 mM [K +] o, respectively). (5) The high K +-induced 86Rb efflux was not practically inhibited by 1 mM tetraethylammonium or 0.1 mM 4-aminopyridine, indicating that the K + channels activated by an elevation of [K +] o are not the delayed (voltage-dependent) K + channels. The present results favoured the conclusion that N-18 cells carry K + channels which open at high [K +] o but are closed at low [K +] o including the physiological range for the mouse neuroblastoma cells (around 5.4 mM). This conclusion leads to the notion that in the mouse neuroblastoma N-18 cells the K + permeability does not mainly contribute to determining the resting membrane potential under physiological conditions.