The long-range goal of this proposal is to identify CNS sites involved in mediating the alcohol deprivation effect (ADE). The long-term ADE is characterized by an increase in baseline alcohol consumption following a deprivation period of one week or longer. The hypothesis of the present proposal is that neuroadaptations occur during a long-term alcohol deprivation which follows chronic alcohol consumption. The [14C]-2-deoxyglucose technique will be used to measure rates of local cerebral glucose utilization (LCGU) to identify CNS regions involved in the alcohol relapse. Adult male rats from the selectively bred alcohol-preferring P line will be used since they readily demonstrate an ADE after deprivation periods of one week and four weeks, following chronic 24-hour alcohol drinking.
The specific aims of this study are to establish the existence of a long-term ADE in animals on a 1-hour scheduled access paradigm and determine LCGU changes associated with the alcohol relapse. The overall purpose of this research is to improve the current understanding of the neurobiological mechanisms underlying alcohol relapse.
