The deleterious effects of prenatal ethanol exposure have been extensively documented in clinical and experimental studies. This paper provides an overview of work conducted with mice to examine the myriad of adverse consequences that result from embryonic/fetal exposure to ethanol. All of the hallmark features of the clinical fetal alcohol syndrome have been demonstrated in mice, including prenatal and postnatal growth retardation, structural malformations and behavioral abnormalities associated with central nervous system dysfunction. As expected, the severity and profile of effects is related to both dosage level and timing of exposure. In addition, these effects have been demonstrated following acute and chronic exposure, with a variety of routes of administration employed. Furthermore, a number of strains have been used in these studies and the variant response (susceptibility) to the teratogenic actions of ethanol exhibited among different mouse strains support the notion that genetic factors govern, at least in part, vulnerability to these effects of ethanol. More recent studies using mouse models have focused on examining potential mechanisms underlying the full spectrum of ethanol's teratogenic actions.