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Adolescent alcohol consumption is prevalent in the United States. Studies report that adolescents ages 12 to 20 consume alcohol at and exceed binge levels, which is defined as 4 drinks for women and 5 for men over two hours. Rodent-model studies considering adolescent intermittent alcohol (ethanol) exposure (AIE) have shown that consumption results in long-term deficits in memory, cognition, social and nonsocial anxiety, and other behaviors into adulthood in part due to the vulnerability of late-developing brain regions such as the frontal cortex, amygdala, and hippocampus. Recent developments have indicated that oxytocin receptor activity is diminished following AIE and that restoration of oxytocin activity can reverse atypical social anxiety, but it is unclear whether oxytocin modulates other AIE-related behaviors. In the current study, Sprague Dawley rats were exposed to ethanol 4 mg/kg during early adolescence from postnatal days (P) 25-45 and then went undisturbed until adulthood (P70-75). During adulthood, a social recognition task was performed to assess short-term memory. We predict that social recognition impairment should be evident in AIE animals compared to non-AIE control subjects. Additionally, as oxytocin receptors are found in multiple brain regions involved in social recognition, we further predict that administering the oxytocin receptor agonist (WAY-267464) will reduce the effects of social recognition impairment in AIE animals. Data is currently being collected and analyzed. Pending results will be presented.



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Assessment of Oxytocin-Receptor Modulation of Social Recognition Following Adolescent Ethanol Exposure