Genetic and environmental factors play a role in the development of
alcoholism. Whole-genome expression profiling has highlighted the importance of several genes that may contribute to
alcohol abuse disorders. In addition, more recent findings have added yet another layer of complexity to the overall molecular mechanisms involved in a predisposition to
alcoholism and addiction by demonstrating that processes related to genetic factors that do not manifest as DNA sequence changes (i.e., epigenetic processes) play a role. Both acute and chronic
ethanol exposure can alter gene expression levels in specific neuronal circuits that govern the behavioral consequences related to tolerance and dependence. The unremitting cycle of alcohol consumption often includes satiation and
self-medication with alcohol, followed by excruciating
withdrawal symptoms and the resultant relapse, which reflects both the positive and negative affective states of
alcohol addiction. Recent studies have indicated that behavioral changes induced by acute and chronic
ethanol exposure may involve chromatin remodeling resulting from covalent histone modifications and DNA methylation in the neuronal circuits involving a brain region called the amygdala. These findings have helped identify
enzymes involved in epigenetic mechanisms, such as the
histone deacetylase,
histone acetyltransferase, and
DNA methyltransferase enzymes, as novel therapeutic targets for the development of future
pharmacotherapies for the treatment of
alcoholism.