Alcoholism is a chronic disorder with severe consequences to physiology of affected individuals, and far- reaching effects on society in general. In particular, further research is required to advance scientific knowledge of the intricate neurobiology underlying the relationship between excessive alcohol drinking and deficits in sleep, a fundamental component of life. This proposal will integrate in vivo measurements of neural calcium activity with electroencephalogram sleep recordings in animal models of long-term, free-choice intermittent heavy alcohol exposure, in order to establish (or refute) causal relationships between the hypothalamic hypocretin system, extended amygdala corticotropin-releasing factor system, and stress-like states of hyperarousal (disrupted sleep) during alcohol withdrawal. Knowledge gained from the proposed experiments will inform future strategies for mitigation of drug abuse and relapse.
Alcohol use disorders present a major public health concern, and these conditions are marked by significant deficits in sleep quality that cause widespread deleterious effects on physiological function. In addition to providing structured opportunities for my professional development, the proposed experiments will advance our understanding of the detailed brain systems that produce alcohol-related sleep disturbances, thereby perpetuating the addiction cycle in genetically-susceptible and/or environmentally-susceptible individuals. Future studies will build upon these findings to improve strategies designed to mitigate drug abuse and relapse.
