Also, in contrast with the Lomitapide Mesylate hypothermia-mediated neuroprotective effects of helium shown to result from the specific heat of helium that is higher than that of air, we found that argon as it could be expected from its specific heat that is half that of air produces mild hyperthermia, a condition well known to worsen ischemic brain damage that could have affected particularly the yet dramatically suffering subcortical brain areas as compared to the cortex. This latter possibility is in line with previous investigations that have shown that, in contrast with the cortex, Dimesna neuroprotection of the striatum is tenuous and can be no longer obtained when time-to-treatment with xenon increases from 1 to 2 h after induction of ischemia or when blood/gas solubility increases from 0.12 to 0.46 as a function of whether xenon or nitrous oxide is used to provide neuroprotection. Finally, if one consider that argon would act by modulating membrane proteins and particularly by potentiating the c-amino-butyric acid type A receptormediated inhibitory neurotransmission, the present finding that postischemic argon provides no improvement of neurologic outcome while reducing cortical but not subcortical brain damage is in good agreement with a recent clinical study that has reported �C in contrast with histological studies in animal models �C that administration after reperfusion of GABAA agonists, but not of anti-cholinergic drugs, disrupts the neuronal plasticity that supports functional recovery in stroke patients and thereby reinduces clinical deficits after stroke. In line with this latter study, it has to be noted that xenon that provides dramatic postischemic neuroprotection possesses efficient antagonistic properties at the cholinergic neurotransmission. It is noteworthy that the lack of neuroprotective effect of argon on ischemia-induced subcortical brain damage reported herein opposes recent data that have demonstrated argon-induced subcortical neuroprotection. Rather than an actual discrepancy, it is likely with little doubt that this can be attributed to major differences in the protocol used. Particularly, administration of argon during ischemia or after ischemia could have played a major role, since previous studies have shown the critical importance of the time inert gases are given, during or after ischemia, to obtain neuroprotection. Also, in contrast with the work by Ryang and colleagues where intraischemic argon was given for 1 h through a face mask in anesthetized rats, in the present study postischemic argon was given for 3 h in freely-moving animals not controlled for temperature in an anesthesia box, an environmental condition shown to allow the effect of inert gases on body temperature to occur much more rapidly than using face mask. Finally, whether neuroprotection by intraischemic argon together with 50 vol% oxygen can be fully attributed to argon remains actually.