Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 124-130). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 124-130). Also available on the Internet.

Thesis (Ph. D.)--University of Texas at Austin, 2003. / Vita. Includes bibliographical references. Available also from UMI Company.

Thesis--Helsinki. / Summary in English. Includes bibliographical references.

Thesis (D. Min.)--Boston University, 2001. / Abstract. Includes bibliographical references (270-277).

Introduction Depression can lead to long term health burden; while alcohol is now also one of the global burdens of diseases. This review is trying to investigate how healthy population can be at risk when the trends of alcohol consumption are increasing. Methods and Results This review studied 11 journals out of 1096 literature in PubMed / Medline / PsyInfo for alcohol and depression association via prospective cohort or longitudinal study. Results varied in outcomes measured and no conclusion on developed causality with alcohol and depression. Discussions Some significant associations may be observed at heavy use of alcohol or binge drinking groups. Young adolescents association was not as significant as adult studies results. Some stratification on gender difference is also non-conclusive. Population on heavy drinking and dependency are at risk of developing depression. Conclusions Future perspectives in research like the need of developing high quality research and more on population approach studies focusing on alcohol and depression should be carried. Prevention of alcohol-related problems especially in young people or population as a whole should include policies reducing overall alcohol consumption, or reducing the rates of high-risk drinking. / published_or_final_version / Public Health / Master / Master of Public Health

Alcoholism is a complex disease that exists as a specific set of behaviors, such as the preoccupation with obtaining alcohol and compulsive alcohol drinking. Currently, more than 18 million adults in the United States suffer from alcohol abuse or alcoholism. This disease poses serious medical and economic consequences for society. Identifying the neurobiological mechanisms that underlie alcohol drinking, specifically the transition from initiation to binge drinking is critical for improved treatments for alcoholics and the vulnerability for relapse in those recovering. Many studies have identified brain regions and molecular mechanisms that underlie various stages of alcohol abuse; however few have investigated the role of specific cell types within these areas. The overarching hypothesis of the studies in this dissertation is that cholinergic interneurons of the nucleus accumbens (NAc) are key neural substrates that underlie alcohol drinking, and as drinking continues; neuroadaptations within these cells then facilitate such behaviors as compulsive alcohol drinking. More specifically, these studies tested whether 1) cholinergic cell ablation in the NAc causes a decrease in alcohol drinking in C57BL/6J mice, 2) neuroadaptive changes in dopamine (DA) D2 receptor and cyclin dependent kinase 5 (Cdk5) occur within these cells following initiation alcohol drinking, and to a greater extent following binge alcohol drinking in C57BL/6J mice, and 3) neuroadaptive changes in DA D2 receptor and Cdk5 also occur in brain regions that have been implicated in the rewarding and reinforcing effects of alcohol in inbred alcohol-preferring (iP) rats. The present findings report a causal role for accumbal cholinergic neurons in binge alcohol drinking and identify DA D2 receptor and Cdk5 neuroadaptations following initiation and binge alcohol drinking. These studies identify the involvement of cholinergic interneurons in binge drinking and reveal alcohol-induced region- and cell-specific receptor and molecular changes that occur with continued drinking. These findings contribute to the understanding of the neurobiological mechanisms that underlie alcohol drinking, and provide the basis for cholinergic targeted treatments designed to attenuate binge drinking. These data also provide the groundwork for future studies aimed to examine receptor and intracellular molecular changes that occur with compulsive alcohol drinking, craving, and relapse.

Alcoholism is a complex disease determined by both genetic and environmental components that exerts a devastating economic and social impact worldwide. The complexity of this disease makes the elucidation of candidate genes for the susceptibility to alcoholism difficult in human populations, however, mouse model systems replicate many aspects of the disease and represent an excellent system for the investigation of the genetic contributions to alcoholism. One component of alcoholism that can be investigated in mouse models is the predisposition to high alcohol consumption. Selectively bred and inbred mice differ markedly in the level of voluntary alcohol intake using a two-bottle choice paradigm. The phenotype of voluntary alcohol consumption in mice is a complex trait and a genetic comparison between mouse models with similar levels of alcohol intake should identify genes that contribute to the predisposition for alcohol consumption. Three different studies were completed at the University of Texas and candidate genes involved in the predisposition to high alcohol consumption in mice were identified through the use of brain transcriptome analysis. In the first study, 3,800 transcripts were identified that were divergent between 3 selected lines and 6 isogenic strains of mice known to differ in voluntary alcohol consumption. This list was filtered to reveal candidate genes associated with alcohol preference on mouse chromosome 9: Arhgef12, Carm1, Cryab, Cox5a, Dlat, Fxyd6, Limd1, Nicn1, Nmnat3, Pknox2, Rbp1, Sc5d, Scn4b, Tcf12, Vps11, Zfp291. In the second study, analysis of voluntary alcohol intake and brain gene expression between two closely related inbred mouse substrains separated for nearly fifty years revealed divergent alcohol consumption as well as genetic variation between the substrains. Finally, the third study revealed dominant and overdominant patterns of expression in an F1 hybrid that voluntarily consumed more alcohol than either inbred parental strain. The microarray datasets analyzed here represent an important first step in the elucidation of the genetic determinants of high alcohol consumption in mice and will be influential in the discovery of genes that play a role in vulnerability to alcoholism in humans.

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