The effects of holothurin A on the resting membrane potential and conductance of squid axon.
The effects of a marine toxin, holothurin A, on the electrical properties of squid axon membranes were studied. External application of holothurin A to the intact axon produced an irreversible depolarization of the membrane to nearly zero potential. Internal perfusion of squid axon with holothurin A produced a biphasic depolarization of the membrane. The time course of the depolarization was much shorter with internal application than with external application. The holothurin A-induced depolarization was partially reversed either by reduction of the external sodium concentration to 1 mM or by removal of sodium from both external and internal solutions. The results demonstrate an increase in resting sodium permeability as one of the mechanisms underlying the depolarization by holothurin A. However, external application of tetrodotoxin had no effect on the membrane depolarization. Increase of the resting permeability to potassium is suggested as the additional mechanism of depolarization. A model is developed which predicts this anomalous depolarization.
D000818:Animals; D001369:Axons / Q000187:drug effects; D049832:Decapodiformes / Q000502:physiology; D006697:Holothurin / Q000494:pharmacology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects*; D009431:Neural Conduction / Q000187:drug effects*; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology; D012503:Saponins / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D009467:Neuromuscular Depolarizing Agents; D012503:Saponins; D006697:Holothurin; D013779:Tetrodotoxin