Neuroapoptosis in the infant mouse brain triggered by a transient small increase in blood alcohol concentration.

Exposure of infant rats or mice to ethanol on a single occasion during the period of rapid synaptogenesis can cause extensive apoptotic neurodegeneration throughout the developing CNS. Prior studies were designed to assess the effects of large doses of ethanol (comparable to heavy binge drinking), whereas in the present study, we sought to determine what magnitude and duration of blood ethanol elevation are required to trigger a minimal neuroapoptotic response. We found that a rise in blood ethanol to a level in the range of 50 mg/dl for a duration of 30 to 45 min was sufficient to trigger a significant neuroapoptosis response deleting approximately 20,000 neurons per infant mouse brain. Since blood ethanol elevations in this range are commonly achieved by humans in a social drinking context, a mother with only a moderate drinking habit might expose her fetus to such elevations on multiple occasions during pregnancy.