Toxicol Lett 1998 Nov 23;100-101:71-6. doi: 10.1016/s0378-4274(98)00167-2.

Post-synaptic inhibitory mechanisms of anaesthesia; glycine receptors.

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(1) The effects on human homomeric alpha1 glycine receptors of 11 general anaesthetics; four barbiturates, two other intravenous anaesthetics, three volatile anaesthetics and two simple gaseous anaesthetics are described. (2) Pentobarbital and thiopental potentiate the current response to bath applied glycine (50 microM) by 200 and 300%, respectively, at clinically relevant concentrations. (3) Neither methohexital nor phenobarbital had any effect on the current response to bath applied glycine (50 microM). (4) Using maximal doses of applied glycine (1 mM) all the barbiturates acted as non-competitive antagonists. (5) Propofol and etomidate potentiate the current response to bath applied glycine (50 microM) by 200 and 10%, respectively, at clinically relevant concentrations. (6) Etomidate acts as a non-competitive antagonist for doses of glycine above the EC50 (197 microM). Propofol was without effect using maximal doses of applied glycine (1 mM). (7) Halothane, chloroform and ether potentiated the response to bath applied glycine (50 microM) by 200, 100 and 200%, respectively, at clinically relevant doses. (8) None of the volatile anaesthetics had any effect using maximal doses of applied glycine (1 mM). (9) Nitrous oxide and xenon potentiated the response to bath applied glycine (50 microM) by 75 and 50%, respectively, at clinically relevant doses. Nitrous oxide also potentiated the response using maximal doses of applied glycine (1 mM). (10) These results suggest a role for glycinergic neurotransmission in the production of anaesthesia.

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