Pharmacological characterization of the voltage-dependent sodium channels of rainbow trout brain synaptosomes.
Batrachotoxin, aconitine, and veratridine, alkaloid activators of voltage-dependent sodium channels, stimulated 22Na+ uptake by rainbow trout brain synaptosomes. The potency and efficacy of activation by these compounds decreased in the following order: batrachotoxin greater than aconitine much greater than veratridine. Aconitine-stimulated sodium uptake was completely inhibited by tetrodotoxin, a specific blocker of voltage-dependent sodium channels. Polypeptide toxins in the venom of the scorpion, Leiurus quinquestriatus, and the insecticide DDT enhanced veratridine-dependent sodium uptake but had no effect on non-specific uptake. These studies identify appropriate conditions for measuring sodium channel-dependent 22Na+ uptake in trout brain synaptosomes and characterize some of the pharmacological properties of trout brain sodium channels. Trout sodium channels differed from those in rat and mouse brain in their responses to batrachotoxin, aconitine, veratridine, and DDT but not to tetrodotoxin and Leiurus venom toxins. These results suggest that the specificity of some of the neurotoxin-binding domains of the trout brain sodium channel may differ from those of sodium channels in mammalian brain.
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000648:ultrastructure; D004594:Electrophysiology; D007473:Ion Channels / Q000187:drug effects* / Q000502:physiology; D009498:Neurotoxins / Q000494:pharmacology*; D009994:Osmolar Concentration; D012964:Sodium / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism* / Q000648:ultrastructure; D014337:Trout
D007473:Ion Channels; D009498:Neurotoxins; D012964:Sodium