Preconditioning-induced ischemic tolerance is one of the most important mechanisms, responsible for the
increased brain resistance after stroke. Recent studies over the past years have provided interesting insights into the
molecular mechanisms of this neuroprotective phenomenon. In this research, we attempted to see changes in the
expression of group I and II metabotropic glutamate receptors (mGluR I and II) following intermittent hyperoxia
preconditioning. Rats were divided into five groups (hyperoxia-intact, hyperoxia-MCAO, room air-intact, room air-
MCAO, room air-sham). Hyperoxia groups were exposed to 95% inspired O2 for 4 h/day and 6 consecutive days. Oxygen
level in room air groups was %21. 48 hours after pretreatment, MCAO-operated groups were subjected to focal cerebral
ischemia for 60 min. 24 hours after reperfusion, neurologic deficit score (NDS) and brain infarct volume (IV) were evaluated
in MCAO-operated subgroups. Sham-operated and intact groups were used to assess expression of group I and II mGluR and
glutathione (GSH) levels of core, penumbra and subcortex regions. The results of this study showed that preconditioning with
intermittent HO decreased NDS and IV, increased GSH levels in subcortex, and upregulated mGluRs I and II significantly.
Although additional studies will be required to further elucidate precise mechanism(s) of ischemic tolerance, it seems that
intermittent HO may exert its protective effects in part through upregulation of mGluR I and II.
Keywords: Brain Ischemia, Glutathione levels, Hyperoxia preconditioning, Ischemic tolerance, Metabotropic glutamate
receptors, Normobaric hyperoxia
Rights & PermissionsPrintExport