Fig. 4. Xenon attenuates N -methyl-D-aspartate (NMDA) receptor-mediated synaptic transmission. NMDA receptor-mediated excitatory postsynaptic currents (NMDA-EPSCs) were recorded with (blue symbols ) and without (red symbols ) 30 μM DL-TBOA, an antagonist of excitatory amino acid transporters. Because extrasynaptic NMDA receptors preferably contain the NR2B subunit, we applied the specific NR2B antagonist Ro-25-6981 (1 μM). Under control conditions, Ro-25-6981 led to a decrease in NMDA-EPSC amplitudes to 53.3 ± 4.9% (95% CI 39.8–66.8; n = 5; P < 0.001). In the presence of DL-TBOA, Ro-25-6981 reduced NMDA-EPSCs to 32.9 ± 5.7% (95% CI 16.9–48.9; n = 5; P < 0.001). This reduction was significantly higher (P = 0.027 for control vs. DL-TBOA), indicating that receptors containing the NR2B subunit have been activated (A ). Xenon decreased NMDA-EPSCs (red symbols ) to 65.9 ± 9.4% (65.9 ± 9.4%; 95% CI 43.1–88.7; n = 7; P = 0.022) compared with control values. Extrasynaptic NMDA receptors were activated by application of DL-TBOA. Under these conditions, xenon reduced NMDA-EPSCs to 58.2 ± 5.8% of control (blue symbols ; 95% CI 44.2–72.2; n = 5; P = 0.004). Each symbol represents the averaged NMDA-EPSC amplitudes ± SEM normalized with respect to the 5-min baseline period before application of xenon or Ro-25-6891 (B ). Period of substance application (black/green bar ). Representative current traces (insets ). § Stimulation artifact.