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

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Abstract
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 μM. 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 (ΔI/Δt) 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.