Fig. 4.
Glycine reverses neuroprotective effect of xenon but not argon. (A) The addition of glycine or the inhibitory glycine receptor antagonist strychnine has no effect on injury development or sham-treated slices. Sham slices (white bars) were not significantly different in the presence of 100 µm glycine (white crosshatched bars) or 100 nm strychnine (white hatched bars) at any time point. Similarly, the development of control injury (grey bars) was not significantly different in the presence of 100 µm glycine (grey crosshatched bars) or 100 nm strychnine (grey hatched bars) at any time point. The error bars are standard errors (N = 141 control traumatic brain injury (TBI); N = 105 sham; N = 39 glycine TBI; N = 35 glycine sham; N = 18 strychnine TBI; N = 19 strychnine sham). (B) Glycine reverses the neuroprotective effect of 50% xenon. In the absence of glycine, 50% xenon (red bars) protects against trauma (grey bars). The addition of 100 µm glycine abolishes the protective effect of 50% xenon. In the presence of glycine, there was no significant difference between injured slices in the absence (grey crosshatched bars) or presence of xenon (red crosshatched bars) at any time point. The error bars are standard errors (N = 141 TBI; N = 104 xenon; N = 32 xenon glycine; N = 39 glycine TBI). (C) Glycine does not reverse the neuroprotective effect of 50% argon. In the absence of glycine, 50% argon (cyan bars) protects against trauma (grey bars). In the presence of 100 µm glycine, 50% argon (cyan crosshatched bars) retains a protective effect compared with injured slices (crosshatched grey bars). The error bars are standard errors. (N = 141 TBI; N = 44 argon; N = 37 argon glycine; N = 39 glycine TBI). *Indicates value significantly different (P < 0.001) from the control injury at each time point. #Indicates value significantly different (P < 0.05) from control injury at each time point.