We address questions related to plasticity in Parkinson’s disease (PD) in mouse models using pharmacologic and genetic approaches to link neuronal activity to PD-relevant behavior, with an emphasis on neuron-type specific pathophysiological changes. Our main projects address the following critical areas:

• how loss of dopamine causes motor dysfunction in part as an aberrant plasticity
• how prolonged pharmacological therapy with levodopa produces restoration of akinesia and also causes dyskinesia
• how the function of basal ganglia output neurons change in each case
• how other neuronal systems interact with the basal ganglia to cause dopamine-resistant symptoms
• the development of disease process-relevant biomarkers to diagnose and differentiate parkinsonian disorders and to monitor disease progression
• understanding the non-motor symptoms of PD such as autonomic dysfunction