Argon possesses oxygen-like properties that could explain at least partly its neuroprotective action. As reported by Semenov, the Nobel Prize Laureate of chemistry in 1956 with Sir Cyril Norman Hinshelwood for their work about branched chain reactions, argon that is incapable of chemical reactions behaves however as a sort of catalyst for some of them by producing a kind of oxygen synergy. In that way, physiological studies have clearly demonstrated that argon at 50 vol% allowed rats exposed to hypoxic 4-(Benzyloxy)phenol conditions incompatible with life to adapt and maintain their oxygen demand Also, argon of 25 to 80 vol% increased survival in rats exposed to normocapnic or hypercapnic hypoxia, and conversely potentiated oxygen-induced convulsions. In addition, in rats exposed to non-lethal hypoxia, argon restored by,35% the mitochondrial respiratory enzyme activity, whose impairment following excitotoxic insults triggers neuronal death. Such a kind of argonoxygen synergism could explain the neuroprotective effects of argon against hypoxia and ischemia as reported in the present and previous studies. Also, since previous data have shown redox modulation of the NMDA receptor with reduction inducing a potentiation and oxidation an inhibition of the NMDA receptor activity and glutamate-induced neuronal death, the synergistic Brusatol effect of argon on oxygen could explain its ability at reducing NMDA-induced neuronal death. Indeed, in line with these data and the ability of argon at reducing NMDA-induced neuronal death, intrainsult oxygen has been shown to have antiexcitotoxic effects and to reduce NMDAinduced neuronal death and intraneuronal calcium influx, a critical event known to play a major role in excitotoxic and ischemic brain damage. In contrast with its beneficial effect at the cortical level, we found that postischemic argon did increase MCAO-induced subcortical brain damage and further failed to reduce MCAOinduced neurologic deficits. This latter effect is in line with previous data that have demonstrated that neuroprotection requires preserving 80�C90% of both the cortex and the subcortical areas to provide significant neurologic recovery and further predicted that 30% of subcortical brain damage might be sufficient to suppress any voluntary motor behavior. Physiologically, the striatum that is the main part of the subcortical brain areas that suffer MCAO-induced brain damage is well recognized to be difficult to protect due to its lack of collateral vasculature and dramatic reduction in cerebral blood flow and oxygen supply as compared to the cortex. In these conditions, the occurrence of argon-induced oxygen synergy would not be possible as it occurs in brain slices exposed to OGD, where oxygen diffusion exists at the air-saline solution interface, in the cortex of rats subjected to MCAO-induced ischemia, where residual oxygen exists due to collateral vasculature, and in the striatum of rats subjected to NMDA injection.