Fig. 4. (A ) Gavestinel (gv) neuroprotection is reversed by adding glycine. Neuroprotection by the prototypical glycine site antagonist gavestinel is attenuated by adding glycine (100 μm). In the absence of added glycine, gavestinel, 0.5 μm (gray bars ) and 5 μm (black bars ) reduces injury to 63 ± 10% and 36 ± 9% of control injury, respectively. Adding glycine abolishes protection by 0.5 μm and 5 μm gavestinel. The error bars are standard errors from an average of 48 slices at each condition. The data have been normalized to the control oxygen-glucose deprivation (OGD) with no added glycine. (B ) Xenon (xe) neuroprotection is reversed by adding glycine. In the absence of added glycine, 50% atm xenon (black bars ) gives robust protection (32 ± 6% of control injury). Adding glycine (100 μm) caused a small, but not significant, reduction in control OGD injury. However, the protective effect of 50% atm xenon was abolished. Addition of the inhibitory glycine receptor antagonist strychnine (100 nm) had no effect on control OGD (with or without glycine), xenon neuroprotection without glycine, or the reversal of xenon neuroprotection by glycine. The error bars are standard errors from an average of 44 slices at each condition. The data have been normalized to the control OGD with no added glycine. * Significantly different (P < 0.05) from control OGD. The four control OGD groups were compared using analysis of variance with Tukey post hoc  test and were not significantly (n.s.) different (P > 0.97).