Halothane inhibits the neurotoxin stimulated [14C]guanidinium influx through 'silent' sodium channels in rat glioma C6 cells.
We have investigated the effect of pharmacological agents on [14C]guanidinium ion influx through sodium channels in C6 rat glioma and N18 mouse neuroblastoma cells. The sodium channels of the N18 cells can be activated by aconitine alone, indicating that they are voltage-dependent channels. In contrast, sodium channels in the C6 cells require the synergistic action of aconitine and scorpion toxin for activation and are therefore characterized as so-called silent channels. The general anesthetic halothane used at clinical concentrations, specifically inhibited the ion flux through the silent sodium channel of C6 rat glioma cells. The voltage-dependent channels of the N18 cells were insensitive to halothane at the concentrations tested.
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D000157:Aconitine / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D004357:Drug Synergism; D005910:Glioma / Q000378:metabolism*; D019791:Guanidine; D006146:Guanidines / Q000378:metabolism*; D006221:Halothane / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D009447:Neuroblastoma / Q000378:metabolism; D009498:Neurotoxins / Q000494:pharmacology*; D051381:Rats; D012604:Scorpion Venoms / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D014701:Veratridine / Q000494:pharmacology
D006146:Guanidines; D007473:Ion Channels; D009498:Neurotoxins; D012604:Scorpion Venoms; D014701:Veratridine; D012964:Sodium; D019791:Guanidine; D006221:Halothane; D000157:Aconitine