Cerebral ischemia and subsequent reperfusion is known to induce irreversible tissue damage with the consequence of more or less pronounced impairments. The underlying cellular and molecular mechanisms however are far from being understood today. In the present study, we employed the well established rat model MCAO (middle cerebral artery occlusion), which uses a unilateral ligature of the middle cerebral artery for a defined period of time, prior to reperfusion. Animals develop symptoms, comparable to stroke in humans. Brains of such animals were used for histochemical and biochemical evaluation of markers, indicating programmed cell death (apoptosis) as evidenced by presence of tissue transglutaminase stained cells, DNA fragmentation and presence of cytochrome c in both cerebral hemispheres ipsilateral and contralateral to occlusion.