Ischemic preconditioning (IPC) of the brain describes the neuroprotection induced by a short, conditioning ischemic episode (CIE) to a subsequent severe (test) ischemic episode (TIE). Most of the supporting evidence for IPC is based on histological assessment, several days after TIE. The aim of this study is to investigate if changes induced by IPC can be detected within 30 min of reperfusion following the ischemic episode. A rat model of "four-vessel occlusion" transient global cerebral ischemia and parametric analysis of electrocorticogram were used. A control group was subjected directly to a 10 min TIE, and in a preconditioned group TIE was induced 48 h after a 3 min CIE. Quantitative histology was performed 48 h after TIE. Our key finding is that, 30 min after reperfusion, there is a significant increase in the electrocortical slow activity in the control group but not in the preconditioned group. Moreover the increase inversely correlates with the degree of electrocortical suppression during seconds 10 to 15 after the onset of the ischemic episode.The tolerance of the brain to an ischemic injury depends not only on the duration and severity of insufficient blood flow but also on various pre-and post-ischemic factors that are able to influence the post ischemic outcome. There is a lot of interest concerning the postischemic factors that can improve the recovery due to immediate clinical applicability. Nevertheless, recent experimental work focuses on the preischemic factors, that can increase the ischemic tolerance, among which the suppression of metabolic rate, the increase of brain tissue energy reserves and the inhibition of membrane permeability of cations are of particular importance [1].One of the most surprising discoveries in the search for preischemic neuroprotective factors was that exposure to short episodes of sublethal insults like ischemia, hypoxia, hyperthermic stresses and toxic agents results in a subsequent resistance to severe ischemic injury. The phenomenon of