RESUMO
Previous studies have demonstrated that Li(+) ions can substitute for Na(+) in a variety of functional systems. Using the single sucrose-gap recording technique, we measured the nerve compound action potential to study the effects of tityustoxin (an alpha-scorpion toxin that selectively inhibits fast Na(+) channel inactivation) upon removal of extracellular Na(+). Our results suggest that tityustoxin requires the presence of extracellular Na(+) to produce its typical pharmacological effect on Na(+) channel inactivation kinetics, but not to bind to its site.
Assuntos
Espaço Extracelular/metabolismo , Neurotoxinas/farmacologia , Nervo Isquiático/efeitos dos fármacos , Venenos de Escorpião/farmacologia , Sódio/metabolismo , Potenciais de Ação/efeitos dos fármacos , Animais , Técnicas In Vitro , Rana catesbeiana , Nervo Isquiático/fisiologia , Bloqueadores dos Canais de SódioRESUMO
We performed the present experiments to study the action of crotamine, a toxin isolated from the venom of the South American rattlesnake, Crotalus durissus terrificus, on macroscopic Na+ currents in frog skeletal muscle by using the loose patch clamp technique. Crotamine at 50 microM increased the peak Na+ current by 50% (P < 0.05). In addition, the voltage dependence of inactivation was shifted by +8 mV. Other parameters of Na+ currents (reversal potential, voltage-dependence of activation and time courses of inactivation, of activation and of removal of inactivation) were not significantly affected. We suggest that crotamine inhibits the direct transition of channels from closed to inactivated states, thereby forcing their transition through the open states.
