Ischemic preconditioning is a neuroprotective mechanism in which a brief non-injurious episode of ischemia protects the brain from a subsequent lethal insult. Recently, it has been reported that modifi ed reperfusion subsequent to a prolonged ischemic episode may also confer neuroprotection, a phenomenon termed postconditioning. Mitogen Activated Kinases (MAPK) play a key role in these neuroprotective mechanisms. Objectives of this study was to evaluate the effect of MAPK activated by preconditioning and postconditioning on the expression of Na+ /Ca2+ exchangers(NCXs), and Acid Sensing Ionic Channels (ASICs), two families of proteins that, by modulating intracellular ionic homeostasis, contribute to the progression of the ischemic lesion. NCX and ASIC protein expression was investigated in rats subjected to harmful ischemia, preconditioning or postconditioning, treated with specifi c MAPK inhibitors or with vehicle alone. Results of this study indicated that NCX1, NCX3 and NCKX2 are up-regulated in those brain regions protected by preconditioning and postconditioning treatment while ASIC1a is downregulated in the same regions. The change observed in the expression of these proteins seems to be due to p-AKT. In fact, p-AKT inhibition reverted the preconditioning and postconditioning neuroprotective effect and prevented NCXs overexpression and ASIC1a downregulation.
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