Prenatal exposure to ethanol is frequently associated with microencephaly, hypomyelinization, delayed cell migration, and impaired neuronal and glial maturation in the offspring. The mechanism by which ethanol induces its effects on the development of the nervous system is still not fully understood. In this study, the influence of acute prenatal exposure to ethanol on the prefrontal cortex cells of rats were examined. Three doses of ethanol (3g/kg of body weight) were administered intraperitoneally to pregnant female rats on the 12th day of pregnancy, at 8 h intervals. Control rats received the same treatment but with a saline solution. Cells in the synthesis phase (S) of the cell cycle were labeled with bromodeoxyuridine. Six controls and 12 ethanol-treated neonates were sacrificed on the 8th day of postnatal life. The distance between nuclear cores in immunohistochemically labeled cells was determined by image analysis. Control rats had a normal neocortex, with six layers in the prefrontal region. Rats treated with ethanol showed ectopia of pyramidal neurons in layers I and II, heterotopia in the basal area of the prefrontal fissure, and a decrease in cellular density in layers II and VI of the cerebral prefrontal cortex. These alterations could help to explain some of the dysfunctions reported in patients with fetal alcohol syndrome.