Peter Brooks

Document Type

Honors Thesis

Publication Date

5-2012

Abstract

The alcohol deprivation effect (ADE) refers to a temporary increase in alcohol intake following a period of alcohol deprivation. Repeated ADE studies (Sinclair & Senter, 1968, Melendez, 2006) have shown that there is an innate tendency to increase consumption when access to alcohol is limited, and the ADE is considered to be an animal model for relapse drinking. The present study is the first to examine the ADE in mice selectively bred for high and low susceptibility for withdrawal seizures, withdrawal-seizure prone (WSP) and withdrawal-seizure resistant (WSR) mice, and the purpose of it was to determine the presence or absence of a correlation between the genetic mechanisms that code for alcohol withdrawal severity and the tendency to increase alcohol consumption with limited access to alcohol. The two different genotypes demonstrated the ADE in two different deprivation schedules and across two different environmental conditions. Because no significant difference in response to intermittent access was found between the WSP and WSR mouse lines, it can be concluded that the phenotypic relapse-like increased drinking when access to alcohol is intermittent (i.e. the ADE) is a result of genetic mechanisms separate from the underlying genetics that code for withdrawal severity.

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