Abstract

I examined the effects of volatile anesthetics and ketamine on the glycine receptor channel expressed in Xenopus oocytes injected with single RNA encoding the α1 subunit of the glycine receptor. The glycine-induced chloride currents in these oocytes were enhanced by 4 volatile anesthetics (halothane, enflurane, isoflurane, and sevoflurane) at clinically relevant concentrations, in a reversible manner. The findings about the effect of halothane on the dose-response curve of the glycine-induced currents suggest that the sensitivity of the recombinant glycine receptor channel was increased by halothane. In contrast, ketamine, an intravenous anesthetic, depressed the glycine-induced currents. These results indicate that both the volatile anesthetics and ketamine modulate the functions of the glycine receptor channel by affecting the αsubunit. Additionally, we examined the effects of these anesthetics on membrane currents in Xenopus oocytes injected with mRNA extracted from the rat brain and spinal cord. Glycine-induced chloride currents in these oocytes were also enhanced by halothane but depressed by ketamine. GABA-induced currents were enhanced both by halothane and by ketamine. Kainate-induced currents were depressed both by halothane and by ketamine. The relevance of the present findings to the mode of action of these anesthetics was discussed.

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