Prenatal binge-like alcohol exposure alters neurochemical profiles in fetal rat brain.

The majority of studies examining the effects of prenatal exposure to alcohol on neurotransmitter levels have furnished results that are divergent (increase, decrease or no change). The present study assessed six neurochemical compounds [norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT), 5-hydroxyindole acetic acid (5-HIAA), gamma-aminobutyric acid (GABA)] from the same brain tissue. Pregnant Sprague-Dawley rats were given 5.1 g/kg alcohol (by gavage) either daily from embryonic day 1 (E1) through E20 or E20 only. In addition, pairfed/intubated (PF/INT) and ad lib chow (Chow) groups were included as controls. The dams were sacrificed and the fetuses were removed on E20. Binge-like alcohol exposure throughout gestation (E1-E20) produced significantly higher brain to body weight ratios compared with all other groups. Alcohol exposure did not produce changes in NE levels, although the E1-E20 exposure to alcohol reduced the contents of DA and 5-HT compared with the PF/INT and Chow controls. In addition, the E20 alcohol treatment reduced both DA and 5-HT levels compared with the E1-E20 alcohol treatment. DOPAC and 5-HIAA contents were affected by the prenatal treatments insofar as the 5-HIAA levels were decreased in E/1-20 and E20 animals relative to both controls, while the DOPAC levels were decreased in E/1-20, E20 and PF/INT groups compared to the Chow group; however, both metabolites were unaffected by the difference in alcohol treatment duration. Moreover, GABA levels were increased in fetuses exposed to alcohol from E1-E20 compared with all other groups. Collectively, these findings suggest that binge-like alcohol exposure prior to and during neurotransmitter development affects the baseline content of several neurotransmitters.