The interactions of the inhalation anesthetic agent isoflurane with to isoflurane. Receptors consisting of/31 and $ y2 subunits were ligand-gated chloride channels were studied using transient not expressed. Isoflurane also enhanced glycine-activated chlo-expression of recombinant human receptors in a mammalian cell ride currents through homomeric a glycine receptors but did not line. Isoflurane enhanced y-aminobutyric acid (GABA)-activated enhance GABA currents in cells expressing homomenc p1 rechloride currents in cells that expressed heteromeric GABAA ceptors. These results show that not all ligand-gated chloride receptors consisting of combinations of al or a2,/31, and 72 channel receptors are sensitive to isoflurane and, therefore, that subunits and in cells that expressed receptors consisting of the anesthetic interacts with specific structural determinants of combinations of only aand 3 subunits. Receptors consisting of these ion channel proteins. a2 and y2 subunits were poorly expressed but were sensitive

It is now accepted that many general anesthetic agents, such human GABAA receptor subunit cDNAs were used for transient expresas barbiturates(1), propofol(2), and the anesthetic steroids sion studies: al, a2, $1, and ‘y2 (8, 14). Also used were the human (3), enhance inhibitory synaptic transmission in the brain via