Prenatal exposure to moderate levels of ethanol can have long-lasting effects on learning and memory in adult offspring

Prenatal alcohol exposure can produce long-lasting cognitive and learning impairments in children. Previous studies have suggested that prenatal ethanol exposure can produce neurochemical abnormalities in hippocampal formation. We examined whether performance in the Morris water task, known to be sensitive to interference with hippocampal function, would be affected in adult offspring of rat darns who consumed moderate levels of ethanol through pregnancy. Rat darns consumed one of three diets throughout gestation: (1) Bio-Serve liquid diet containing 5% ethanol (v/v; 26% EDC), which produces a maternal peak blood ethanol concentration of 100 mg/dl; (2) pair fed an isocalorically equivalent amount of 0% ethanol liquid diet; or (3) laboratory chow ad Libitum. Adult offspring from each of the three maternal diet conditions were brained in one of three versions of the Morris water task. We employed the "standard" fixed hidden platform task, the moving platform task, and a task that measures competition between cue and place navigation. All three groups learned to navigate normally in the fixed hidden platform version and showed clear preferences for the goal location during no-platform probe trials. In contrast, in the moving platform version and the cue versus place competition task, the prenatally exposed rats were abnormal relative to the rats of the other two maternal diet conditions. In both of these tasks, they behaved in a manner consistent with the idea that acquisition of new place information does not proceed as effectively as in normal rats. These data are consistent with the hypothesis that hippocampal circuitry and neurochemistry related to synaptic plasticity are important targets underlying at least some of the long-lasting deleterious cognitive effects of prenatal alcohol exposure.