Microencephaly and hyperactivity in adult rats can be induced by neonatal exposure to high blood alcohol concentrations.

To investigate whether or not blood alcohol concentration during the brain growth spurt has an influence on the permanency of alcohol-induced central nervous system damage, an artificial rearing technique was used to administer a daily dose of alcohol (6.6 g/kg/day) to neonatal rats during postnatal days 4 to 10. The alcohol was administered either in a condensed pattern over 8 h resulting in cyclic blood alcohol concentrations with high peaks, or uniformly over each 24-h period resulting in stable, but low peaks. The condensed alcohol exposure resulted in considerable microencephaly (20% to 25%), with significant growth deficits in the cerebrum, cerebellum, and brain stem of rats of either sex at day 10; there still was significant microencephaly (16% to 19%) in adult rats that received the condensed alcohol exposure as neonates. Furthermore, activity at day 90 in rats of either sex that had condensed alcohol exposure was elevated compared with that of the gastrostomy control group. In contrast, the rats having uniform alcohol exposure had only nonsignificant changes in brain weight both on day 10 and day 90 and did not exhibit hyperactivity at day 90. Thus, neonatal alcohol exposure producing high blood alcohol concentrations caused permanent deficits in brain growth and significant changes in activity, whereas the same daily dose of alcohol administered in a pattern that resulted in consistently low blood alcohol concentrations failed to produce either permanent microencephaly or increased activity. These data support the hypothesis that patterns of alcohol exposure that produce high concentrations in the blood, such as "binge-drinking," increase the risk of permanent damage to the developing brain.