Prenatal alcohol exposure disrupts male adolescent social behavior and oxytocin receptor binding in rodents.

Social behavior deficits resulting from prenatal alcohol exposure (PAE) emerge early in life and become more pronounced across development. Maturational changes associated with adolescence, including pubertal onset, can have significant consequences for social behavior development, making adolescence a unique period of increased vulnerability to social behavior dysfunction. Unfortunately, little is known about the underlying neurobiology supporting PAE-related social behavior impairments, particularly in the context of adolescence, when the transition to a more complex social environment may exacerbate existing deficits in social behavior function. Here we perform a comprehensive evaluation of social behavior development in PAE animals during two different periods in adolescence using three separate but related tests of social behavior in increasingly complex social contexts: the social interaction test, the social recognition memory test (i.e. habituation-dishabituation test), and the social discrimination test. Additionally, we investigated the underlying neurobiology of the oxytocin (OT) and vasopressin (AVP) systems following PAE, given their well-documented role in mediating social behavior. Our results demonstrate that compared to controls, early adolescent PAE animals showed impairments on the social recognition memory test and increased OT receptor binding in limbic networks, while late adolescent PAE animals exhibited impairments on the social discrimination test and increased OTR binding in forebrain reward systems. Taken together, these data indicate that PAE impairs adolescent social behavior - especially with increasing complexity of the social context - and that impairments are associated with altered development of the OT but not the AVP system.