Effect of sea anemone toxins on the sodium inactivation process in crayfish axons.
The effect of sea anemone toxins from Parasicyonis actinostoloides and Anemonia sulcata on the Na conductance in crayfish giant axons was studied under voltage-clamp conditions. The toxin slowed the Na inactivation process without changing the kinetics of Na activation or K activation in an early stage of the toxin effect. An analysis of the Na current profile during the toxin treatment suggested an all-or-none modification of individual Na channels. Toxin-modified Na channels were partially inactivated with a slower time course than that of the normal inactivation. This slow inactivation in steady state decreased in its extent as the membrane was depolarized to above -45 mV, so that practically no inactivation occurred at the membrane potentials as high as +50 mV. In addition to inhibition of the normal Na inactivation, prolonged toxin treatment induced an anomalous closing in a certain population of Na channels, indicated by very slow components of the Na tail current. The observed kinetic natures of toxin-modified Na channels were interpreted based on a simple scheme which comprised interconversions between functional states of Na channels. The voltage dependence of Parasicyonis toxin action, in which depolarization caused a suppression in development of the toxin effect, was also investigated.
D000818:Animals; D003400:Astacoidea; D001369:Axons / Q000502:physiology*; D003064:Cnidarian Venoms / Q000494:pharmacology; D004553:Electric Conductivity; D006706:Homeostasis; D007473:Ion Channels / Q000187:drug effects; D008387:Marine Toxins / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism / Q000502:physiology*; D013997:Time Factors
D003064:Cnidarian Venoms; D007473:Ion Channels; D008387:Marine Toxins; C027605:parasicyonis toxin; C028800:toxin II (Anemonia sulcata); D012964:Sodium