title: How Gymnodinium breve red tide toxin(s) produces repetitive firing in squid axons.
abstract: Partially purified toxin(s), GbTX, extracted from Gymnodinium breve red tide organisms elicits a spontaneous train of action potentials in the squid giant axon. The spikes have a shape similar to that in the normal seawater control except for an increase in the rate of recovery from the afterhyperpolarization. With this more rapid recovery, the membrane potential overshoots the resting potential and  threshold, triggers another spike, and thus produces repetitive firing. Voltage-clamp studies revealed that the toxin has no effect on the normal sodium or potassium conductance changes produced by step depolarization. However, consistent with the faster recovery after an action potential, GbTX speeds recovery of the "shut-off" currents to their steady-state values after a depolarization. The most likely mechanism by which the toxin accelerates recovery after an action potential (leading to repetitive firing) is the induction of a small additional inward current which was found to be reduced by prehyperpolarization. This toxin-induced current which speeds recovery is blocked by tetrodotoxin and hence presumably flows through the sodium channel.
mesh_terms: D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001369:Axons / Q000187:drug effects* / Q000378:metabolism; D049832:Decapodiformes; D004141:Dinoflagellida; D056890:Eukaryota; D066298:In Vitro Techniques; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D008954:Models, Biological; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D014118:Toxins, Biological / Q000494:pharmacology*
chemical_list: D014118:Toxins, Biological; D012964:Sodium; D011188:Potassium