The present study has possible weaknesses that must be discussed. First, although there is no real alternative to use an anesthetic such as isoflurane to induce transient brain ischemia, the impact of isoflurane administration in combination with 100 vol% oxygen on the findings of this study must be examined. Indeed, since isoflurane is known as a neuroprotectant preconditioning agent in the adult but not in the newborn rat, it is possible that residual isoflurane could have contributed at least partly to provide neuroprotection against MCAO-induced cortical brain damage. Conversely, it is possible that residual isoflurane could have contributed to increase MCAO-induced subcortical brain damage by producing apoptosis, an adverse L-Ornithine effect of isoflurane yet demonstrated when given in combination with nitrous oxide but not alone. Likewise, since oxygen has been shown either to reduce or to increase excitotoxic and/or ischemic brain damage, it is possible that the use of 100 vol% oxygen to induce isoflurane anesthesia could have contributed also to reduce cortical brain damage and/or to increase subcortical brain damage. However, these possibilities are unlikely to be true since in the present study the total duration of surgery was no more than 25 minutes, thereby allowing rapid isoflurane and oxygen desaturation from the rat’s body and brain and thereby the virtual absence of residual isoflurane and oxygen during the period of treatment with argon; isoflurane was never given in combination with argon. Support for this are previous data with the same protocol that have shown that xenon, in contrast with what found in the present study with argon, provides neuroprotection both at the cortical and subcortical levels. Second, in this study, cerebral blood flow was not measured throughout MCAO since we wanted to shorten anesthesia to limit isoflurane effects. However, this should not have Metaproterenol Sulfate biased our results since postischemic argon obviously induces neuroprotective and adverse effects at the cortical and subcortical level respectively. Indeed, it is unlikely that such a dichotomic response could be attributed to a technical problem of occlusion/reperfusion, which if such should have biased data in the same way at the cortical and subcortical level. In conclusion, our results do not support that postischemic argon could be an efficient alternative to xenon, shown to provide dramatic postischemic neuroprotection. However, given its antiexcitotoxic effect, it is possible that argon could be useful for treating other brain insults, such as brain trauma. M. bovis has been shown to persist in the environment for several months to years, raising questions about the role of environmental reservoirs in the chronic persistence of bTB in some cattle herds and wildlife populations. Reservoirs of infection have been reported in wildlife populations in parts of the United Kingdom, Republic of Ireland, North America, Africa and New Zealand.