Date of Award

Spring 2015

Degree Type


Degree Name

Doctor of Philosophy (PhD)


Psychological Sciences

First Advisor

Julia A. Chester

Committee Chair

Julia A. Chester

Committee Member 1

Susan E. Swithers

Committee Member 2

Steve L. Boehm

Committee Member 3

Edward A. Fox


Chronic stress exposure during adolescence is associated with more long-lasting negative consequences than exposure during adulthood. Adolescent chronic stress exposure has long-lasting effects on physiology and behavior, including an increased risk of developing an alcohol use disorder (AUD) later in life. This relationship is particularly true in individuals with a familial history of AUDs. Recent research has shown that chronic stress in adolescent mice increased voluntary alcohol consumption in adulthood, but did not do so in adult mice. However, little is known about the mechanism of the relationship between adolescent chronic stress and increased alcohol consumption in adulthood. Evidence suggests that chronic stress exposure during adolescence has long-term effects on the developing brain, including areas important for sensitivity to the rewarding effects of alcohol. The over-arching aim of the current study was to explore the effects of adolescent chronic stress on sensitivity to the motivational effects of alcohol in adulthood. Three stress treatment groups were used, including subjects exposed to stress during adolescence, subjects exposed to stress during adulthood, and subjects not exposed to stress. Within each stress treatment group, high-alcohol preferring (HAP2) and low-alcohol preferring (LAP2) mice were represented, to mimic differences in familial AUD history. Thirty days after stress exposure, all subjects began a conditioned place preference (CPP) paradigm, a behavioral task that measures the sensitivity to alcohol's rewarding effects. Since re-exposure to a stressor has been associated with an increased risk in relapse and other drug-seeking behaviors, half of the subjects in each stress treatment group were re-exposed to the original stressor (RS) before the CPP posttest. Overall, LAP2 mice showed greater CPP than HAP2 mice, which supports more recent literature suggesting that an inverse relationship between alcohol consumption and CPP expression may exist. In contrast to what was hypothesized, adolescent stress exposure decreased CPP expression in the HAP2 subjects during the first portion of testing. This finding may support an inverse relationship between alcohol consumption and CPP expression, when interpreted such that subjects exposed to stress during adolescence may drink more during adulthood because they are less sensitive to the rewarding effects of alcohol. In LAP2 subjects, there were no differences in CPP expression between the stress treatment groups, supporting past research suggesting that HAP2 mice are more sensitive to alterations in drug-related behaviors following stress exposure. RS did not produce alterations in CPP in either line. Overall, the findings of the current study suggest that one explanation for why individuals exposed to stress during adolescence may increase alcohol consumption during adulthood might be because more alcohol is required in order to reach the desired perceived rewarding effects of the drug, especially in those with a familial history of AUDs.