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Alcohol is frequently co-administered with other psychotropic substances, yet little is known about patterns of alcohol use in a simultaneous polysubstance context. In the present dissertation concomitant alcohol-drug administration is examined with an emphasis on delineating patterns of alcohol use when it is co-administered with psychostimulant drugs known to interact with neural mechanisms believed to be involved in mediating alcohol's ascending limb reinforcing effects: midbrain dopamine transmission. / In two retrospective self-report studies polysubstance users reported on their simultaneous use of drugs and alcohol. Results revealed that alcohol was commonly co-administered with various abused substances, particularly with psychostimulant drugs that are known to increase dopamine neurotransmission, and there was an identifiable pattern of administration that was characterized by initial alcohol consumption preceding repeated intermingled alcohol-psychostimulant administrations which resulted in alcohol dose escalation. / In a third study, the effects of administering the psychostimulant drug nicotine on alcohol intake was directly examined using a double-blind placebo controlled self-administration procedure. Nicotine was found to significantly increase alcohol ingestion. / In a final study we examined the effect of decreasing dopamine neurotransmission on alcohol self-administration by using a dietary manipulation that depletes the nutritional precursors to dopamine. This procedure was found to decrease alcohol consumption, an effect that was especially evident in a subset of drinkers thought to be hypersensitive alcohol's ascending limb dopamine effects. Overall findings suggest that alcohol co-administration with psychostimulant drugs affects patterns of alcohol intake and that this may be the result of an interaction involving dopamine neurotransmission.

Alcoholism is a prevalent multifactorial disease with both genetic and environmental components. Monoamine oxidase (MAO) has been proposed as a susceptibility marker for familial alcoholism but consistent evidence of either specific MAO variants in alcoholics or allelic segregation in at-risk families has not been presented. Two structural genes on the X chromosome encode two forms of the enzyme, MAO-A and MAO-B. Kinetic constants for platelet MAO-B and restriction fragment length polymorphisms for MAO-A were determined in alcoholics with multigenerational family histories of alcoholism, high risk relatives of familial alcoholics and low risk controls with no family history of alcoholism. Mean elevated levels of MAO-B deamination were observed in alcoholics and high risk individuals. Alcoholic and high risk individuals did not differ from non-alcoholics with respect to MAO-B tryptamine affinity or MAO-A polymorphisms. Significant non-genetic factors influence MAO-B activity. MAO variants are unlikely to define a genetic predisposition to alcoholism.

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Thesis (M.S.)--Auburn University, 2007. / Abstract. Vita. Includes bibliographic references (ℓ. 40-44)

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Thesis (M.A.)--Humboldt State University, 2007. / Includes bibliographical references (leaves 34-38). Also available via Humboldt Digital Scholar.

Thesis (Ph.D.) -- University of Adelaide, Dept. of Clinical and Experimental Pharmacology, 2000. / Bibliography: leaves 246-263.

Thesis (Ph.D.)--University of Rhode Island, 2007. / Includes bibliographical references (leaves 93-106).