The effects of a toxin (ATX II) from the sea anemone Anemonia sulcata on the electrical and mechanical activity of the denervated hemidiaphragm of the rat.

Isolated strips of rat diaphragm denervated 9-21 days prior to experimentation were used to study the effects of the sea anemone toxin ATX II on electrical and mechanical activity in mammalian skeletal muscle. ATX II increased twitch tension transiently and induced a concentration-dependent rise in muscle tone. The resting membrane potential was increased to more negative values by low concentrations of ATX II (greater than or equal to 2 x 10(-7)M). ATX II at 10(-7)M prolonged the action potential duration, however, individual fibres exhibited a large variation in response. Lidocaine (5 x 10(-5)M) reversed the toxin-induced contracture, but did not inhibit the ATX II-induced prolongation of action potential duration. ATX II increased the incidence of spontaneous action potentials which occur in denervated skeletal muscle. This effect was partially reversed by tetrodotoxin (10(-6)M), which also partially abolished the ATX II-induced contracture. Reduction in toxin-induced spontaneous activity was also observed in the presence of lidocaine (5 x 10(-5)M) or acetylcholine (10(-5)M). Both agents diminished ATX II-induced contracture. It is concluded that the increased muscle tone observed with ATX II may reflect a summation of increased fibrillatory activity.