Given the crucial roles for the major protein targets of drugs of abuse in shaping brain development ( Bhide, 2009 Bonnin and Levitt, 2011 Frederick and Stanwood, 2009 Hohmann, 2003 Kater and Lipton, 1995 Lauder, 1993 Money and Stanwood, 2013 Stanwood and Levitt, 2004), it should not be surprising that fetal drug exposures have been linked to a wide variety of brain deficits. Substance use disorders among pregnant women continues to be a major public health concern, posing risk to the child’s development, and imposing socioeconomic burdens on society by increasing needs for medical and social services. Modern mechanistic approaches have informed us greatly as to how to potentially ameliorate the induced deficits in brain formation and function, but conclude that better delineation of sensitive periods, dose–response relationships, and long-term longitudinal studies assessing future risk of offspring to exhibit learning disabilities, mental health disorders, and limited neural adaptations are crucial to limit the societal impact of these exposures. Early studies of fetal exposures focused on classic teratological methods that are insufficient for revealing more subtle effects that are nevertheless very behaviorally relevant. We focus both on animal models and available clinical and imaging data from cross-sectional and longitudinal human studies. In this review, we describe current knowledge on how alcohol, nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) produce alterations in neurodevelopmental trajectory. ![]() These effects on the developing nervous system, before homeostatic regulatory mechanisms are properly calibrated, often differ from their effects on mature systems. In utero exposures to drugs thus can have long-lasting implications for brain structure and function. Most drugs of abuse easily cross the placenta and can affect fetal brain development.
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