The Effect of Prenatal Cocaine Exposure on Vocalizations and Brain Development in Infant Pups (2011)

Undergraduate: Amy Abramowitz

Faculty Advisor: Josephine Johns
Department: Psychology & Neuroscience

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Crying in humans and ultrasonic vocalizations (USVs) in rats during the neonatal period elicit maternal retrieval and care in mothers. By postnatal day (PND) 21 juvenile rats developing normally decrease vocalizing behavior when isolated from their litter. Studies suggest prenatal cocaine exposure (PCE) in both human and rodent neonates coincide with abnormal development of crying behaviors. This abnormal crying might increase the risk of caregivers neglecting their infants. Using a rat model of PCE (a model for prenatal insult, drug exposure, and postnatal neglect) the molecular mechanisms contributing to aberrant neonatal vocalizing behavior can be explored. In this study several acoustic features of USVs in rodent pups on PND 21 were analyzed following chronic prenatal cocaine injections, chronic saline injections, or in litters left untreated. The neurobiological mechanisms potentially underlying USV alterations were also explored. Results suggest that rats prenatally exposed to cocaine or saline continue to exhibit a robust vocalizing behavior through PND 21, a time when pups typically stop vocalizing. Neuronal maturation of the ventromedial hypothalamus (VMH), the area responsible for vocalizations produced in response to pain, was also increased in rats exposed to cocaine, however linear regression analysis found no relationship between VMH development and vocalizing differences observed. This suggests a delay in normal developmental stages of language following PCE.