Understanding the processes which control ethanol self- administration is of primary importance in eventual treatment and prevention of alcohol abuse and alcoholism. The nature and biological mechanisms of ethanol's reinforcing properties are central to the overall understanding of this intake control. Recently, a neural basis for reward has been postulated to be important for a variety of abused drugs. The role which this neural system plays in ethanol reinforcement and intake has yet to be thoroughly explored. The proposed studies will begin to examine the role which this brain reward system may play in ethanol self- administration. A biological model will be used in which oral ethanol self- administration is initiated without the need for food or water deprivation. When the animals are orally self-administering ethanol, a variety of agonists and antagonists active at either dopaminergic, GABAergic or benzodiazepinergic receptor sites will be injected directly into specific brain loci to determine their affect on self-administration. The drugs to be tested are halo- peridol, apomorphine, muscimol, bicuculine, chlordiazepoxide and an inverse benzodiazepine agonist. The brain areas of interest are the nucleus Accumbens, caudate putamen, the ventral tegmental area (A10), the substantia nigra and the ventral pallidum. Control animals, orally self-administering either sucrose only or concurrently administering ethanol and sucrose, will also be examined using the same procedures used for ethanol self-admini- stration. Comparison of these three self-administration conditions will allow for an initial determination of the role which the postulated brain reward system may play in ethanol self- administration.
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