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Background
I obtained my HBSc and PhD at the University of Toronto in Canada. During my graduate work with Dr. José Nobrega, I studied deep brain stimulation (DBS) applied to the basal ganglia in models of movement disorders. Using molecular biology, neuroimaging, neurochemistry and behavioral pharmacology, I investigated the neural mechanisms underlying the adverse psychiatric effects and therapeutic motor effects of DBS.
For post-doctoral training, I moved to the lab of Dr. Christian Lüscher at the University of Geneva in Switzerland. Here, I used optogenetics and electrophysiology to understand how cocaine drives adaptations in the ventral basal ganglia circuitry, and how these adaptations contribute to the diverse symptoms of addiction. Using this insight, I developed a novel protocol for DBS that reversed cocaine-evoked synaptic plasticity in the nucleus accumbens and abolished maladaptive behavior induced by cocaine exposure.
In order to treat any condition, we must first understand its underlying pathology. To this end, my research interest seeks to integrate a variety of approaches to understand how plasticity in the ventral basal ganglia mediates behaviors such as reward-seeking, risk tolerance and hedonic valuation of rewards. My ultimate goal is to develop neuromodulation strategies that would regulate basal ganglia circuit function in models of mood, chronic pain and substance-use disorders, and could be used to treat symptoms of these conditions.
I obtained my HBSc and PhD at the University of Toronto in Canada. During my graduate work with Dr. José Nobrega, I studied deep brain stimulation (DBS) applied to the basal ganglia in models of movement disorders. Using molecular biology, neuroimaging, neurochemistry and behavioral pharmacology, I investigated the neural mechanisms underlying the adverse psychiatric effects and therapeutic motor effects of DBS.
For post-doctoral training, I moved to the lab of Dr. Christian Lüscher at the University of Geneva in Switzerland. Here, I used optogenetics and electrophysiology to understand how cocaine drives adaptations in the ventral basal ganglia circuitry, and how these adaptations contribute to the diverse symptoms of addiction. Using this insight, I developed a novel protocol for DBS that reversed cocaine-evoked synaptic plasticity in the nucleus accumbens and abolished maladaptive behavior induced by cocaine exposure.
In order to treat any condition, we must first understand its underlying pathology. To this end, my research interest seeks to integrate a variety of approaches to understand how plasticity in the ventral basal ganglia mediates behaviors such as reward-seeking, risk tolerance and hedonic valuation of rewards. My ultimate goal is to develop neuromodulation strategies that would regulate basal ganglia circuit function in models of mood, chronic pain and substance-use disorders, and could be used to treat symptoms of these conditions.