Alcohol use disorders (AUDs) are characterized by the loss of control over alcohol consumption and the emergence of negative emotionality during abstinence from alcohol. AUDs affect 16 million people in the United States alone and alcohol misuse represents the first risk factor for premature death and disability in young adults worldwide. Current treatment options for AUDs include three FDA-approved medications as well as behavioral therapies, but AUDs have a high rate of relapse even in treated individuals. There is a dire need for more efficient therapeutic strategies and a deep understanding of the neurobiological mechanisms mediating the behavioral symptoms of AUDs is a prerequisite for the rational development of targeted therapies.
While the brain regions and neurotransmitter systems affected by chronic alcohol exposure are well characterized, our understanding of the specific neural circuits and molecular events driving drinking escalation and negative affect during withdrawal remains limited.
The Contet laboratory seeks to fill this gap of knowledge by identifying molecular and circuit mechanisms that causally contribute to the behavioral symptoms of AUDs. To achieve this goal, our projects combine behavioral models of excessive alcohol drinking in mice with genetic engineering methods enabling the manipulation of gene expression and neuronal activity.