Dr. Robert Schmidt Bernstein Center Freiburg – The European Neuroscience Institute in Freiburg

  • Young Investigator

Computational Models of Motor Control in the Basal Ganglia

About Dr. Robert Schmidt

Motor control faces a dilemma: quick responses can be necessary for survival, but premature or impulsive responses can have devastating consequences. Our brain has evolved to maintain a balance between these extremes. In some neurodegenerative diseases this balance seems to be disturbed. For example, patients with Parkinson´s disease have problems initiating voluntary movements, as if a system that is usually meant to inhibit premature or impulsive behaviors has become too strong and now dominates most motor output.

Current treatments of neurological disorders such as deep brain stimulation for Parkinson´s disease are limited by our understanding of the activity and the function of the target regions. In previous work studied neural circuits involved in movement initiation and cancellation by comparing activity in multiple basal ganglia structures in rats performing a stop-signal task [1]. Subthalamic nucleus (STN) neurons showed low latency responses to Stop cues, irrespective of whether actions were successfully canceled or not. By contrast, neurons downstream in the substantia nigra pars reticulata (SNr) responded to Stop cues only when actions were successfully suppressed. Remarkably, SNr neurons with fast Stop cue responses formed a functionally-defined ´hotspot´ that corresponds to the anatomically-defined SNr "dorsolateral core" region. Recordings and computational modeling together indicate that sensorimotor gating of the stop cue arises in the hotspot from the relative timing of two distinct inputs to SNr: cue-related excitation from STN and movement-related inhibition from striatum.

In addition to these spiking patterns, we found evidence for beta oscillations being important when sensory cues are utilized for behavior [2]. Usually beta oscillations are considered as pathological activity in Parkinson´s Disease. However, we found transient epochs of beta in healthy rats performing different choice tasks, indicating a functional role in basal ganglia processing. Specifically, cue-induced increases in beta power only occurred for cues that are ‘used’, for example, after the Stop cue on Correct but not Failed Stop trials.

At the new BrainLinks-BrainTools research cluster I plan to develop a new generation of computational models that describe the rich movement-related activity patterns we observed in different basal ganglia subregions. These models will help to distinguish healthy from pathological activity patterns (e.g. in Parkinson´s disease) and help to devise more sophisticated treatment strategies (e.g. algorithms for closed-loop deep brain stimulation).

For further information, please see: http://www.brainlinks-braintools.uni-freiburg.de/who-we-are/people/profile-schmidt?set_language=en

Awards, Fellowships and Honours 

2013-            Junior Research Group Leader Grant from the CoE BrainLinks-BrainTools (Exc 1086)

2011            2-year DFG postdoc grant (until end of 2012)

Technical Expertise

  • Neural Basis of Behavior, Memory and Learning
  • Basal Ganglia Pathways for Action Selection, Initiation, Inhibition and Execution
  • Dopamine and Reward-Related Learning
  • Hippocampal Phase Precession, Temporal Coding and Oscillations