Anemonia sulcata toxins modify activation and inactivation of Na+ currents in a crayfish neurone.
The effects of three toxins (ATX I, II, III) isolated from the sea anemone Anemonia sulcata were studied in the soma membrane of a crustacean neurone under voltage-clamp conditions. 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 microM. In the presence of ATX the Na+ inactivation was incomplete even with pulses of 700 ms length or strong depolarizing prepulses. Besides the effects on the inactivation process ATX affected also the activation of the Na+ current. In cells treated with ATX the negative resistance branch of the peak Na+ current voltage relation was shifted by -5 mV to -20 mV. The time to peak was increased for small depolarizations (up to -30 mV) and the rate of rise (delta I/delta t) was enlarged by ATX. A slow activating current component was also observed after depolarizing prepulses or if the Na+ current was outward. 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. 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.
Hartung
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K
Rathmayer
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W
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003400:Astacoidea; D003064:Cnidarian Venoms / Q000494:pharmacology*; D004553:Electric Conductivity; D007473:Ion Channels / Q000187:drug effects*; D009046:Motor Neurons / Q000187:drug effects*; D012964:Sodium / Q000378:metabolism*
D003064:Cnidarian Venoms; D007473:Ion Channels; D012964:Sodium