Date Thesis Awarded

5-2010

Access Type

Honors Thesis -- Access Restricted On-Campus Only

Degree Name

Bachelors of Science (BS)

Department

Neuroscience

Advisor

Pamela S. Hunt

Committee Members

Robert C. Barnet

Deborah C. Bebout

Randolph A. Coleman

Mark H. Forsyth

Abstract

A focus on early development is critical for understanding the etiology of alcoholism. The observation that alcoholism runs in families has strengthened the idea of a genetic basis for the disease. It is also recognized, however, that growing up in a household where alcohol cues are omnipresent may provide critical experiences that could increase that risk. The effects of early experience with ethanol cues can be examined using the demonstrator-observer paradigm in rats. During the early postnatal period, experimental subjects (observers) were exposed to intoxicated siblings (demonstrators) in their home cage. Controls were exposed to sibling demonstrators that were administered water. Animals were tested for voluntary ethanol intake (Experiments 1, 2a, 3 and 4) or ethanol odor preference (Experiment 2b) when they reached an age corresponding to early adolescence in humans, postnatal day 30. Results revealed that infant experience with ethanol cues in the home environment resulted in increased ethanol intake and ethanol odor preference by adolescent-age subjects. These responses to alcohol were not only evident in observer subjects, but in the demonstrator animals as well (Experiments 2a and 2b). Thus, both direct (intoxication) and indirect (via siblings) exposure to ethanol cues in the home environment can increase animals' preferences for this drug. Experiment 3 was designed to evaluate whether a reactivation treatment (exposure to ethanol odor) prior to a test for ethanol ingestion would increase the expression of the ethanol preference. Results of this experiment failed to reveal such an effect. Finally, Experiment 4 evaluated the hypothesis that the endogenous opioid system is involved in this type of social learning. Observer subjects were injected with the mu opioid antagonist naltrexone prior to interactions with intoxicated siblings. Results failed to support our hypothesis. Observers injected with naltrexone ingested just as much ethanol during the intake test as those that were injected with saline. Collectively, the results of these experiments indicate that social interactions with an intoxicated conspecific early in development are critical experiences impacting later ethanol ingestion. The findings from these experiments emphasize the important influence of early social experiences on later behavioral responses toward ethanol, and suggest that this type of ethanol exposure can have long-lasting consequences. Early learning about alcohol in the context of the home environment may result in increased risk for the later development of alcohol abuse and dependence.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

Comments

Thesis is part of Honors ETD pilot project, 2008-2013. Migrated from Dspace in 2016.

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