The effects of maternal alcohol consumption on the levels and metabolism of neurotransmitters in offspring are reviewed. In addition, studies of CNS myelination and hepatic lipids are discussed. In utero exposure to ethanol is reported to alter the steady-state levels, metabolism or release of catecholamines, octopamine, serotonin, glutamate, GABA, acetylcholine and histamine. However, with the exception of a deficit of hypothalamic norepinephrine and a deficit of whole brain serotonin, most of the neurotransmitter alterations appear to be either transient or were detected when ethanol was present in the fetus or neonatal animals. There are conflicting reports on the effect of pre- and early postnatal exposure to ethanol on CNS myelination in the rat. However, it appears that if ethanol and control rats were of comparable body weights, there were only minor differences in myelination. Nonetheless, if the rat mothers consumed ethanol for 1 1/2--2 months prior to conception and during gestation, the offspring had increased myelin early in development. An examination of hepatic lipids in the fetal and neonatal rats that were exposed to ethanol in utero and at the time of sacrifice demonstrated an increased concentration of hepatic lipids and decreased fatty acid oxidation. The discussion of the neurotransmitter, myelin and hepatic lipid studies include an assessment of the nutritional status of the animals and the permanence of any observed abnormalities.