Ciguatera fish poisoning is a distinctive form of ichthyosarcotoxism characterised mainly by gastrointestinal and neurological disturbances. The ciguatoxins, responsible for this poisoning, are complex polyethers produced by toxic strains of the dinoflagellate Gambierdiscus toxicus. These toxins are increased to dangerous levels for man during their transmission through herbivorous and carnivorous fish, various species being contaminated. The known molecular target of ciguatoxins is the voltage-gated Na+ channel. During the action of these toxins, the permanent opening of channels, at the resting membrane potential, produces a continuous entry of Na+ ions in excitable cells causing a marked increase in membrane excitability and in cellular volume. To precise the neurocellular basis of the efficacy of some agents used in clinical and traditional treatments of ciguatera, their effects were studied on frog myelinated axons exposed to Pacific ciguatoxin-1B (CTX-1B). During the action of this toxin, the increase in axonal volume and membrane excitability was reversed by lidocaine (a local anaesthetic), by CaCl2 and by hyperosmotic external solutions (containing D-mannitol, sucrose tetramethylammonium chloride). The CTX-1B induced hyperexcitability of the membrane was also reversed by extracts of Argusia argentea leaves or Davallia solida rhizomes, used traditionally in New Caledonia. It is concluded that the various agents studied are able to counteract the neurocellular effects of CTX-1B in myelinated axons. These results are of particular interest since they provide a scientific basis to understand the beneficial action of therapeutic agents used in the treatment of ciguatera fish poisoning.