Anemonia sulcata toxins modify activation and inactivation of Na+ currents in a crayfish neurone

1. The effects of three toxins (ATX I, II, III) isolated from the sea anemoneAnemonia sulcata were studied in the soma membrane of a crustacean neurone under voltage-clamp conditions. 2. All three toxins affected the action potentials and the Na⁺ currents in a similar manner. The lowest concentrations tested (10 nM, 20 nM and 50 nM for AtX I, II and III, respectively) had pronounced selective effects on the Na⁺ current. No effect on K⁺ or Ca²⁺ currents was observed with concentrations up to 5 M. 3. In the presence of ATX the Na⁺ inactivation was incomplete even with pulses of 700 ms length or strong depolarizing prepulses. 4. Besides the effects on the inactivation process ATX affected also the activation of the Na⁺ current. 5. In cells treated with ATX the negative resistance branch of the peak Na⁺ current voltage relation was shifted by –5 mV to –20 mV. 6. The time to peak was increased for small depolarizations (up to –30 mV) and the rate of rise (I/t) was enlarged by ATX. A slow activating current component was also observed after depolarizing prepulses or if the Na⁺ current was outward. 7. The decay of the Na⁺ tail currents was considerably prolonged after the application of ATX if the membrane was repolarized to potentials more positive than about –60 mV. 8. Repetitive stimulation led to a shortening of the action potential in ATX II treated neurones. A simultaneous and parallel decrement of the peak and plateau current was observed with depolarizing voltage steps.