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In the offspring of ethanol-treated rats during gestation (25% ethanol in drinking water) decreased litter size, increased postnatal mortality rate, reduced body weight and body size, delayed ear opening, eyelid opening and teeth eruption, retarded air righting reflex acquisition, impaired brain growth, reduced cortical thickness and delayed maturation of layer Vth's pyramidal neurons: reduced basilar dendritic arborization and decreased number of spines in the apical dendrite, were observed when compared with age-matched controls fed with a standard diet. Minimal effects were found in the offspring of fibre-treated rats during gestation (standard diet mixed with cellulose) in which the body weight was similar to that of controls, although both the calorific intake from food and the mother's weight gain during pregnancy were similar to those of the ethanol-treated group. All these abnormal parameters became normal at the end of the first month of postnatal life, indicating recovery of these developmental defects produced by prenatal ethanol consumption.

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To increase our understanding of the effects of chronic ethanol consumption beginning at adolescence, 25% ethanol in drinking water (v/v) was administered daily to young rats aged 45-50 days for 5 months. Increased numbers of dendritic spines on the apical dendrite of layer V pyramidal neurons of the somatosensory cortex (U-Mann-Whitney test, P less than 0.01-0.05) were found in almost every 50-micron-long segment over a distance of 500 microns from the cell body in ethanol-treated rats at the age of 195-200 days when compared with age-matched controls. Although the mechanisms leading to this unusual finding are not know, it is suggested that impairment of the naturally occurring elimination of redundant synapses can not be ruled out.

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Some aspects of small intestine maturation have been studied in the newborns from chronic ethanol-treated pregnant rats (25% ethanol in drinking fluid) immediately after birth (before suckling) and after 30 days of life. Litters delivered by mothers fed ad libitum with a standard diet diluted 50% with cellulose were used as a nutritional control. At birth, pups from ethanol-treated mothers showed significant decreases in total intestinal length and thickness, low total lactase activity and low somatostatin intestinal content. The intestinal alterations of these neonatal parameters are not present in newborns from mothers on fiber-diluted diet. From delivery, pups from different experimental groups were nursed by normal lactating dams. At 30 days of age neither of those parameters differed among the groups. We propose that the low levels of total lactase activity in newborns from alcoholic mothers, that are a consequence of a lower intestinal mucosa content, are a direct effect of ethanol in utero on the fetal gastrointestinal system.