MAR 16, 2016 12:00 PM PDT

Featured Speaker - Striatal Synaptic Dysfunction in Parkinson's disease

Presented At Neuroscience
C.E. CREDITS: P.A.C.E. CE
Speakers
  • Chair, Department of Physiology, Nathan Smith Davis Professor of Physiology, Professor in Physiology, Northwestern University, Feinberg School of Medicine
    Biography
      Dr. James Surmeier is the Nathan Smith Davis Professor and Chair of the Department of Physiology at the Feinberg School of Medicine at Northwestern University and Director of the Morris K. Udall Research Center of Research Excellence for Parkinson's Disease at Northwestern University. Dr. Surmeier received his PhD in Physiology and Biophysics from the University of Washington in 1983. He trained with leaders in the field of neurophysiology, including Dr. Arnold Towe, Dr. William Willis and Dr. Stephen Kitai. In 1998, he moved to the Department of Physiology at Northwestern University and assumed his current position in 2001.

      Dr. Surmeier's research program focuses on the ionic mechanisms underlying neural activity in the basal ganglia and their modulation by activation of G-protein coupled receptors, particularly those for dopamine. He has pioneered the application of modern patch clamp and single cell gene profiling approaches to understanding basal ganglia physiology, authoring over 100 peer-reviewed publications in journals such as Science, Nature, Neuron, Nature Neuroscience and the Journal of Neuroscience.

      Dr. Surmeier has served in several advisory capacities lo the National Institutes of Health, including chairing study sections for NINDS and acting as a Councilor for NIAAA. He also serves on the scientific advisory boards of the Hereditary Disease Foundation, Dystonia Foundation and the Tourette Syndrome Association and a number of editorial boards. He has received many scientific awards including the NARSAD Established Investigator award, the Riker Award, the Picower Foundation Award and the Jacob Javits Neurosciencc Investigator Award.

    Abstract:

    Traditional models of basal ganglia disorders are grounded in the assumption that network dysfunction is driven by alterations in intrinsic excitability of striatal neurons. Recent work has challenged this assumption, showing that in mouse models of Parkinson’s disease there are profound alterations in synaptic strength and connectivity accompanying network pathophysiology. The talk will summarize this work in two steps. The first part of the talk will give a basic overview of basal ganglia structure and function, emphasizing the complementary roles of direct and indirect pathways in regulating goal directed and habitual movement. New insights into the cortical and thalamic connectivity of striatal direct and indirect pathway spiny projection neurons (SPNs) will be outlined along with the mechanisms governing their strength. The second part of the talk will provide a summary of work characterizing cell-specific alterations in the number and strength of synaptic connections driving SPN activity in the hypokinetic parkinsonian state and after administration of levodopa at doses sufficient to produce hyperkinetic dyskinesia. The interplay of homeostatic and dopamine-dependent synaptic plasticity in shaping these alterations in synaptic function will be examined and an attempt made to reconcile synaptic changes with the hypokinetic and hyperkinetic features of these states. Translational opportunities arising from these insights also will be mentioned.


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