Anemonia sulcatatoxin (ATX II) enhances spontaneous electrical activity and tension in chronically denervated rat diaphragm

Abstract

In isolated strips of rat diaphragm denervated 9-21 days prior to experimentation, spontaneous action potentials were recorded extracellularly and twitch and resting tension were measured. The sea anemone toxin ATX II enhances the occurrence of spontaneous action potentials, increases resting tension and depresses twitch tension. These effects are essentially irreversible. In low sodium solution substituted with sucrose the effects of ATX II are attenuated, however, they fully develop upon return to normal sodium solution with a marked transient increase in the incidence of spontaneous action potentials and in resting tension. ATX II remains uneffective after pretreatment with tetrodotoxin. Reelevation of the extracellular sodium concentration after exposure to low sodium solution per se causes a marked increase in occurrence of fibrillation potentials, however the transient increase in resting tension was much smaller than in the presence of ATX II. Substitution of chloride with the impermeable anion methylsulphate enhances spontaneous activity and resting tension without an effect on twitch tension. Addition of ATX II elevates resting tension although the concomitant further increase in incidence of spontaneous action potentials is small. It is concluded that the increase in resting tension reflects a summation of the fibrillatory activity, but fibrillations become more effective when the preparations are exposed to ATX II. This finding points at the possible rôle of sodium ions in excitation contraction coupling of denervated skeletal muscle.