Sodium depletion in the periaxonal space of the squid axon treated with pyrethroids.
Pyrethroids are known to increase the steady-state sodium current during a step depolarization and to increase and prolong the tail sodium current associated with a step repolarization of the membrane. The pyrethroid-induced tail sodium current of squid axons developed as a function of the duration of the conditioning depolarizing pulse. However, with further lengthening the conditioning pulse duration, it decreased, further increased, or remained constant depending on the direction of sodium current during the depolarization, irrespective of the membrane potential per se. The depletion or accumulation of sodium in the periaxonal space during a 200-ms conditioning depolarizing pulse in the axon internally treated with pronase, pyrethroids, or both, was demonstrated by measurements of the changes in sodium reversal potential. Thus the observed changes in tail current amplitude as a function of the conditioning pulse duration are explicable in terms of changes in sodium concentration in the periaxonal space without assuming inactivation of the pyrethroid-modified channel.
D000818:Animals; D001369:Axons / Q000187:drug effects*; D049832:Decapodiformes; D005110:Extracellular Space / Q000378:metabolism; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials; D026023:Permethrin; D011722:Pyrethrins / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*
D007473:Ion Channels; D011722:Pyrethrins; D026023:Permethrin; D012964:Sodium; C051001:cyphenothrin