University of California, San Francisco
University of Oxford
University of Cambridge
Wolfram Schultz is a graduate in medicine from the University of Heidelberg. After postdoctoral stays in Germany, USA and Sweden, and a faculty position in Switzerland, he works currently at the University of Cambridge. He combines behavioural, neurophysiological and neuroimaging techniques to investigate the neural mechanisms of rlearning, goal-directed behaviour and economic decision making. He uses behavioural concepts from animal learning theory and economic decision theories to study the neurophysiology and neuroimaging of reward and risk in individual neurons and in specific brain regions, including the dopamine system, striatum, orbitofrontal cortex and amygdala.
University of Calgary
University of California, Davis
Dalton James Surmeier
Professor and Chair, Department of Physiology
Feinberg School of Medicine, Northwestern University
Chicago, Illinois, United States
Dr. D. James Surmeier is the Nathan Smith Davis Professor and Chair of the Department of Physiology at the Feinberg School of Medicine at Northwestern University. Dr. Surmeier received his Ph.D. in Physiology and Biophysics from the University of Washington. He trained with leaders in the field of neurophysiology, including Dr. Arnold Towe, Dr. William Willis and Dr. Stephen Kitai. He assumed his current position as Chair of the Department of Physiology at Northwestern University in 2001. Using an array of cutting-edge approaches, Dr. Surmeier’s research program focuses physiological determinants of Parkinson’s and Huntington’s diseases. His work has uncovered basic mechanisms underlying neural activity in the basal ganglia and how it is perturbed in these disease states. His work has identified the molecular determinants of network dysfunction in both diseases, paving the way for novel pharmacological and genetic therapies. His pursuit of the mechanisms underlying selective neuronal vulnerability in Parkinson’s disease has led to the identification of activity-dependent calcium entry through Cav1 Ca2+ channels as a primary trigger for mitochondrial oxidant stress in at-risk neurons, providing a potential explanation for the selective vulnerability of substantia nigra dopaminergic neurons –neurons whose loss underlies the cardinal motor symptoms of Parkinson’s disease. Corroborated by epidemiological studies, this discovery study has led to a major Phase III clinical trial in North America to determine the ability of the dihydropyridine isradipine to slow the progression of early stage Parkinson’s disease.