Toxin-induced K+ efflux through the Na+ channel of neuroblastoma cells.
Neurotoxins which modify the gating system of the Na+ channel in neuroblastoma cells and increase the initial rate of 22Na+ influx through this channel also give rise to the efflux of 86Rb+ and 42K+. These effluxes are inhibited by tetrodotoxin and are dependent on the presence in the extracellular medium of cations permeable to the Na+ channel. These stimulated effluxes are not due to membrane depolarization or increases in the intracellular content of Na+ and Ca2+ which occur subsequent to the action of neurotoxins. The relationships of 22Na+ influx and 42K+ (or 86Rb+) effluxes to both the concentration of neurotoxins and the concentration of external permeant cations strongly suggest that the open form of the Na+ channel stabilized by neurotoxins permits an efflux of K+ ions. Our results indicate that for the efflux of each K+ ion there is a corresponding influx of two Na+ ions into the Na+ channel.
D000818:Animals; D003064:Cnidarian Venoms / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008433:Mathematics; D008564:Membrane Potentials / Q000187:drug effects; D009447:Neuroblastoma / Q000378:metabolism*; D009498:Neurotoxins / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D012615:Sea Anemones; D012964:Sodium / Q000378:metabolism*; D014701:Veratridine / Q000494:pharmacology
D003064:Cnidarian Venoms; D007473:Ion Channels; D009498:Neurotoxins; D014701:Veratridine; D012964:Sodium; D011188:Potassium