OHSU

Graduate Studies Faculty

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Verginia C. Cuzon Carlson, Ph.D.

Assistant Scientist
Admin Unit: Oregon National Primate Research Center
Phone: 503-629-4151
Lab Phone: 503-629-4085
Office: West Campus - Cooley Building
Mail Code: L583
Programs:
Behavioral Neuroscience
Neuroscience Graduate Program
Research Interests:
electrophysiology; fetal alcohol spectrum disorders; alcohol abuse; basal ganglia; brain development; synaptic plasticity
Preceptor Rotations
Academic Term Available Spring 2014 Unknown
Faculty Mentorship
Dr. Cuzon Carlson is available as a mentor for 2014-2015.
Profile

Research in the Cuzon Carlson laboratory focuses on how mature and developing neuronal circuits are modulated by drugs of abuse, particularly alcohol.  Our long-term goal is to contribute to the understanding of addiction and fetal alcohol spectrum disorder (FASD) in order to reveal novel routes of therapeutic interventions for individuals with FASD or struggling with alcoholism. We focus on brain areas such as the dorsal striatum that are involved in cognition, decision-making, and behavioral control that contribute to addiction. The laboratory uses a multidisciplinary approach including molecular biology techniques, patch clamp electrophysiology, genetic approaches using optogenetics and transgenic mouse lines, and behavioral paradigms to address our two overarching questions.

Our first area of emphasis is to understand the neural mechanisms that underlie the transition from acute drug exposure to chronic exposures that lead to addiction, tolerance, and dependence. To this end we want to gain a better understanding of the cellular and molecular mechanisms of GABAergic and glutamatergic synaptic plasticity in the striatum, and its role in action-outcome and stimulus-response learning that we hypothesize plays a role in the development of addiction. We have examinated the effects of chronic ethanol exposure in multiple animal models including “Drinking in the Dark” and chronic intermittent exposure to ethanol via vapor in mice, as well as ethanol drinking for over a year in a non-human primate model. From these studies, it has been revealed that the GABAergic system in the dorsal striatum is particularly susceptible to the effects of ethanol. Moving forward, we plan to use to advantage transgenic mouse lines and optogenetic technology in order to test the hypothesis that specific GABAergic synapses are more susceptible to the effects of ethanol exposure than others within the subregions of the dorsal striatum.

The second question examines the development of dorsal striatal circuitry and how teratogens, such as alcohol, disrupt normal circuit development. For this project, we use a mouse model that mimics exposure to ethanol spanning the entire human gestational period. We examine the effect of fetal alcohol exposure on GABAergic and glutamatergic neurotransmission and synaptic plasticity of the dorsal striatum as well as their contribution to behavioral abnormalities observed in Fetal Alcohol Spectrum Disorder, such as altered decision making processes, are determined.

By examining the effects of alcohol, we hope to gain insight on normal basal ganglia development and the basal ganglia circuitry involved in normal behaviors such as decision-making and associative learning. Ultimately, we hope to reveal novel routes of therapeutic interventions for individuals with FASD or struggling with alcoholism.