Fig. 8. Enflurane depresses both N -methyl-d-aspartate (NMDA) receptor– and non-NMDA receptor–mediated inward currents evoked by glutamate application. Experiments were done in the presence of tetrodotoxin, with both γ-aminobutyric acid A and glycine inhibitory chloride channels blocked by their respective antagonists, bicuculline (20 μm) and strychnine (2 μm); control and washout were with antagonists present in the artificial cerebrospinal fluid. (A ) In the presence of the NMDA receptor antagonist D,L-2-amino-5-phosponopentanoic acid (50 μm), glutamate evoked inward currents presumably through non-NMDA receptors. Enflurane reversibly depressed these currents. (B ) Enflurane depressed inward currents if non-NMDA receptors were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (10 μm). The depressant effect was reversible. Glutamate was applied at the time indicated by the arrows.