title: Effect of sea anemone toxins on the sodium inactivation process in crayfish axons.
abstract: 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.
mesh_terms: 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
chemical_list: D003064:Cnidarian Venoms; D007473:Ion Channels; D008387:Marine Toxins; C027605:parasicyonis toxin; C028800:toxin II (Anemonia sulcata); D012964:Sodium