Our laboratory uses molecular, genetic, anatomical and behavioral approaches to determine the contribution of the basal ganglia and cerebellum to normal movements and movement disorders. Our specific interest is the pathophysiological basis of dystonia, a movement disorder characterized by abnormal patterns and strengths of muscle contractions caused by dysfunction of the basal ganglia, the cerebellum or both. We manipulate specific subpopulations of neurons using genetically engineered mice, viral vectors or region-specific drug injections by targeting ion channels, receptors or neurotransmitters to induce or ameliorate dysfunction. Then, we assess the effects of these manipulations on the motor behavior of mice, allowing us to pinpoint the molecular or cellular source of the dysfunctional signal. By using a cross-disciplinary approach, we have developed several mouse models of dystonia, which has lead to a better understanding of the disorder and to the development of a drug discovery program.