Joshua Dudman received his Ph.D. at Columbia University, where he worked with Dr. Steven Siegelbaum. In collaboration with Dr. Eric Kandel he examined the role of HCN ion channels in regulating the physiology and plasticity of hippocampal and cerebellar circuits. In his Ph.D. studies he also described a non-Hebbian, heterosynaptic form of plasticity in hippocampus - part of an ongoing expansion of our understanding of diverse forms of plasticity mediated by complex dendritic integration of synaptic inputs. Following graduate school Dr. Dudman joined the Janelia Research Campus of the Howard Hughes Medical Institute first as a Fellow and now as a Group Leader. The Dudman Lab uses a combination of imaging, electrophysiology, behavior and computational modeling to study the role of basal ganglia circuits in controlling purposive behaviors. In addition the lab aims to develop and apply hardware, software, and molecular tools for neuroscience.
Whether learning how vigorously to push a child on a swing or how long to persist in waiting for a train to arrive, we often learn how to perform actions to achieve a desired purpose. This learning occurs through experience - the history of purposive actions and the resultant outcomes. Our lab is interested in understanding the neural circuits in the brain that mediate this ubiquitous form of learning. Specifically, we seek to define key computations and their biophysical mechanisms that underlie these adaptive changes in purposive behavior. In our lab we have recently focused on a critical nexus in the mammalian brain where sensory information, reinforcement signals, and motor commands come together to subserve purposive actions - basal ganglia. During my seminar I will focus on our understanding of how basal ganglia contribute to learning of two behavioral paradigms that require mice to use prior experience to control the vigor and/or persistence of actions. I will describe a set of data that integrate cell-type specific manipulation of plasticity, electrophysiological recordings of neural population dynamics, detailed behavioral assessment of learning, and quantitative modeling. Using this data I articulate a common computation in basal ganglia circuits that appears to underly the control of both vigor and persistence of purposive action. I will also show that this computation is dramatically and specifically impaired in Parkinson’s disease due to the depletion of midbrain dopamine neurons. The conservation of basal ganglia circuits throughout the entire vertebrate lineage suggests that this computation may represent a “canonical” circuit mechanism by which basal ganglia circuits control how voluntary actions are executed.