A wide variety of drugs and chemicals elicit neurobehavioral teratogenesis. Surprisingly, however, despite the obvious differences among unrelated compounds, the behavioral outcomes often display striking similarities, such as cognitive and attentional deficits. Recent studies of drugs of abuse (heroin, nicotine, barbiturates) and environmental toxins (environmental tobacco smoke, pesticides, metals) suggest that, regardless of the originating mechanism for perturbation of brain development, disparate neuroteratogens converge downstream on common families of alterations, characterized by changes in the expression and/or activity of the cell-signaling molecules that are essential to neuronal differentiation and synaptic communication. Identification of these common targets may help in the design of pharmacologic interventions that, administered in adulthood, can reverse the impact of exposure to neurobehavioral teratogens.