Acute ethanol exposure during late mouse neurodevelopment results in long-term deficits in memory retrieval, but not in social responsiveness.

objectivePrenatal alcohol exposure can result in neurological changes in affected individuals and may result in the emergence of a broad spectrum of neurobehavioral abnormalities termed fetal alcohol spectrum disorders (FASD). The effects of ethanol exposure during development are both time and dose dependent. Although many animal models of FASD use more chronic ethanol exposure, acute developmental alcohol exposure may also cause long-lasting neuronal changes. Our research employed behavioral measures to assess the effects of a single early postnatal ethanol intoxication event in mice. MATERIALS AND

methodsMice were dosed at postnatal day 6 (a 2.5 g/kg dose of ethanol or a saline control administered twice, 2 hr apart) as a model of third trimester binge drinking in humans. This exposure was followed by behavioral assessment in male mice at 1 month (1M) and at 4 months of age (4M), using the Barnes maze (for learning/memory retrieval), exploratory behavior, and a social responsiveness task.

resultsEthanol-exposed mice appeared to be less motivated to complete the Barnes maze at 1M, but were able to successfully learn the maze. However, deficits in long-term spatial memory retrieval were observed in ethanol-exposed mice when the Barnes maze recall was measured at 4M. No significant differences were found in open field behavior or social responsiveness at 1M or 4M of age.

conclusionsAcute ethanol exposure at P6 in mice leads to mild but long-lasting deficits in long-term spatial memory. Results suggest that even brief acute exposure to high ethanol levels during the third trimester equivalent of human pregnancy may have a permanent negative impact on the neurological functioning of the offspring.