Three kinetically distinct potassium channels in mouse neuroblastoma cells.
1. Mouse neuroblastoma cells were utilized to examine the electrical properties of single K+ channels which might underlie multiple components of outward current in vertebrate neurones. The conductance, kinetics of activation, inactivation, and pharmacology of three types of channels were compared. 2. Two types of voltage-dependent channels, primarily permeable to K+, were identified which did not require the presence of internal Ca2+. The first had gating kinetics best classified as a delayed rectifier. The conductance of the open channel was 35 pS (22 degrees C) in solutions having symmetrical 125 mM-K+ concentrations. 3. The second type of channel had a conductance of 14 pS under identical conditions. The gating kinetics of this type of channel were distinct from those of the delayed rectifier. The mean first latency, and lifetime of the open state at any voltage, were longer. The maximum probability of an open channel was smaller, so that this parameter appeared less sensitive to the membrane potential. The rate of inactivation of the channel was slower. Further, at the more negative membrane potentials tested, the level of steady-state inactivation was less for this type of channel. 4. The delayed rectifier channel was more sensitive to the blocking action of 4-aminopyridine than the channel with low conductance. 5. A Ca2+ -activated, voltage-dependent K+ channel, having a conductance of 140 pS, was also identified. The maximum probability of an open channel increased, and the voltage for half-maximal activation shifted to a more negative potential as the internal Ca2+ was increased. 6. The time course of inactivation of K+ currents recorded from the whole cell declined in two phases, probably due to the presence of the two types of voltage-dependent K+ channels.
Quandt
F N
FN
Department of Medical Physiology, University of Calgary, Faculty of Medicine, Alberta, Canada.
D015761:4-Aminopyridine; D000200:Action Potentials / Q000187:drug effects; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D051379:Mice; D009447:Neuroblastoma / Q000503:physiopathology; D011188:Potassium / Q000502:physiology*; D014407:Tumor Cells, Cultured / Q000502:physiology*
D000631:Aminopyridines; D007473:Ion Channels; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium