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.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Specialized Center (P50)
Project #
5P50AA017823-04
Application #
8381983
Study Section
Special Emphasis Panel (ZAA1-BB)
Project Start
Project End
Budget Start
2012-09-01
Budget End
2013-08-31
Support Year
4
Fiscal Year
2012
Total Cost
$87,670
Indirect Cost
Name
State University of NY, Binghamton
Department
Type
DUNS #
090189965
City
Binghamton
State
NY
Country
United States
Zip Code
13902
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Lovelock, D F; Deak, T (2017) Repeated exposure to two stressors in sequence demonstrates that corticosterone and paraventricular nucleus of the hypothalamus interleukin-1? responses habituate independently. J Neuroendocrinol 29:
Gano, Anny; Doremus-Fitzwater, Tamara L; Deak, Terrence (2016) Sustained alterations in neuroimmune gene expression after daily, but not intermittent, alcohol exposure. Brain Res 1646:62-72
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