Alcohol use by human adolescents is pervasive, with over 10% of 8th graders, 20% of 10th graders and 25% of 12th graders reporting consumption of five or more drinks in a row in the past two weeks. High levels of alcohol consumption may be fostered in adolescents in part because of their insensitivity to certain desired ethanol effects as well as to effects of ethanol used to self-monitor intake, whereas these relatively high intakes may exacerbate certain adverse ethanol effects to which adolescents may be unusually sensitive. Indeed, animal studies have shown adolescents to differ considerably from adults in their sensitivity to acute ethanol, with these alterations bi-directional in nature. Though less sensitive than adults to many ethanol effects (e.g., sedative, motor-impairing and anxiolytic effects), adolescents are conversely more sensitive than their adult counterparts to ethanol-induced social facilitation and ethanol-related impairments in LTP and spatial memory. Recent work has shown that these effects are particularly pronounced during early adolescence, with animals of this age varying considerably in their ethanol sensitivities from older adolescents and adults. Using an established animal model of adolescence and animals generated from the ANIMAL CORE, the proposed work will examine factors contributing to the unique mosaic of behavioral sensitivities to ethanol seen in young adolescents. Psychopharmacological studies will explore contributions of developmental alterations in GABAA and NMDA receptor systems to an ethanol effect for which young adolescents are unusually sensitive (social facilitation) as well as for consequences of ethanol to which they are relatively resistance (anxiolysis and behavioral suppression) when compared with older adolescents and adults. Using the NEUROANATOMY CORE, additional studies will examine ontogenetic patterns of regional brain activation undergoing transformation during adolescence, and determine whether pharmacological manipulations that block age-related behavioral responses to ethanol likewise attenuate age-specific patterns of ethanol-induced cFos activation in target regions of interest.

National Institute of Health (NIH)
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
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Special Emphasis Panel (ZAA1-BB)
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State University of NY, Binghamton
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