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Cocaine use in women is correlated with child neglect and abuse. Young children prenatally exposed to cocaine are reported to exhibit early signs of neurobehavioral stress and decreased response to caregivers. It is reasonable to suggest that drug-exposed infants seeking comfort from a non-nurturing caretaker might have difficulty responding to their mother/caretaker because of direct neurobehavioral effects following prenatal cocaine exposure (PCE). Animal models of cocaine-induced maternal neglect suggest rodent mothers from both drug-treated and control groups exhibit disrupted offspring-induced maternal behavior towards cocaine-exposed neonates. Results support human studies and suggest cocaine-induced changes in both mother and offspring influence the quality of maternal care and hence developmental outcome of the infant although little is understood about the mechanisms underlying these effects. Work presented here employed parallel translational studies examining behavioral responses of drug-treated mothers, their drug-exposed infants, and neurobiological mechanisms underlying behavioral differences in both human and animal models. Cries were elicited in cocaine-exposed and control human infants at one month of age and subsequently examined for variations in cry acoustics. Mothers returned to lab at three months postpartum and were tested for perceptual response to naturally occurring cries. An animal model of PCE was employed examining if PCE results in similar acoustic variations during the neonatal period and if these differential acoustic properties influence a rodent mother's preference-like behavior. Additionally, our rodent model was used to explore early brain development in PCE and control rodent offspring during early neonatal and juvenile periods. Findings suggest in human and rodent neonates PCE affects early mother-infant interactions in part through changes in infant-produced vocalizations and that gestational cocaine-exposure in human and rodent mothers affects maternal responsiveness to those stimuli. Additionally results suggest variations in neuronal developmental in the Central Amygdala and Ventral Medial Hypothalamus may contribute to variations in vocalizations in juvenile but not infant rodents. These studies provide both translational value, assessment of human and rodent offspring vocalizations and maternal response, and possible mechanisms underlying behavioral effects in offspring. The objectives serve to determine how cocaine affects development in PCE offspring, nurturing behavior in mothers, and long-term offspring developmental outcome.