An ischemic insult to the brain evokes cell damage which may progress to cell death. We invariably associated cell death with necrosis. Necrosis exhibits well defined morphological characteristics, and the biochemical and biophysical processes associated with necrosis have been identified. However, another form of cell death exists, apoptosis. Apoptosis plays an important role in the early development of tissues. Cells undergoing apoptosis exhibit very different morphological characteristics and temporal profiles of change from cells undergoing necrosis. Apoptosis has been identified with the internucleosomal fragmentation of DNA. More importantly, apoptosis has been associated with a process of programmed cell death, in which a genetic program is activated which results in the death of the cell. In this presentation, we will review our data on the morphological, biochemical and molecular evidence of apoptosis in the rodent (rat, mouse) brain after middle cerebral artery occlusion. Emphasis will be placed on describing the temporal profile and the anatomical distribution of cells undergoing apoptosis as functions of duration of MCA occlusion and reperfusion after MCA occlusion. This possible contribution of selective genes in promoting and/or inhibiting apoptosis will also be discussed.