Our research focuses on identifying the neurobiological basis of neuropsychiatric disorders, such as alcohol use disorders. We investigate the cellular and circuit alterations that occur in areas of the brain in response to excessive, pathological alcohol consumption. We are particularly interested in changes that occur in specific populations of neurons and in specific afferent projections to these neurons. We are also interested in contributions of these changes to excessive, pathological alcohol consumption. The result of the research will guide future efforts toward the development of more effective therapeutics for alcohol use disorders.
Using a combination of slice electrophysiology, optogenetics and chemogenetics, transgenic animals, and neuropharmacology, we currently investigate alcohol-mediated aberrant plasticity in the dorsal striatum, a major entry structure of the basal ganglia. The dorsal striatum is crucial for expression of habit and goal-directed behaviors that has recently been linked to addiction. The dorsal striatum receives a number of different glutamatergic inputs, including corticostriatal and amygdalostriatal afferents, and also contains two groups of principal neurons: dopamine D1 or D2 receptor-expressing medium spiny neurons (D1 or D2 MSNs, respectively). We are interested in elucidating how different afferent glutamatergic inputs in distinct types of neurons within the dorsal striatum are altered by excessive alcohol intake, and how such alterations contribute to excessive alcohol-drinking behaviors.