Fetal alcohol syndrome (FAS) was first defined in the early 1970s as a pattern of growth

retardation, facial anomalies, and mental retardation in infants born to alcoholic women

(Jones & Smith, 1973). Children with FAS show distinctive and persistent outcomes,

including sometimes-subtle patterns of cognitive dysfunction (e.g., Jacobson & Jacobson,

1994; Roebuck, Mattson, & Riley, chapter 1, this volume; Streissguth et al., 1991;

Streissguth et al., 1994). Researchers developed animal models to characterize the

phenomenology, pathology, and risk factors associated with maternal alcohol

consumption during pregnancy (Abel & Hannigan, 1995; Chen & West, chapter 2, this

volume; Chernoff, 1997; Driscoll, Streissguth, & Riley, 1990). In vivo whole animal

models of specific structural alcohol-related birth defects (ARBDs) and of the recently

defined alcohol-related neurodevelopmental disorders (ARNDs; Stratton, Howe, &

Battaglia, 1996) successfully met those goals (Randall, 1987; Schenker et al., 1990). The

biological and neurobehavioral sequelae of prenatal alcohol exposure in animals can be

remarkably consonant with the clinical and behavioral outcomes in humans (Abel, 1984;

Driscoll et al., 1990; Roebuck et al., chapter 1, this volume).