The Role of inhibition in generating and controlling Parkinson’s disease oscillations in the basal ganglia
- 1 Bernstein Center Freiburg, University of Freiburg, Germany
- 2 Department of Neurobiology and Biophysics, University of Freiburg, Germany
- 3 Computational Neuroscience, University of Freiburg, Germany
Movement disorders in Parkinson’s disease (PD) are commonly
associated with slow oscillations and increased synchrony of neuronal
activity in the basal ganglia. The neural mechanisms underlying this
dynamic network dysfunction, however, are only poorly understood. Here,
we show that the strength of inhibitory inputs from striatum to globus
pallidus external (GPe) is a key parameter controlling oscillations in
the basal ganglia. Specifically, the increase in striatal activity
observed in PD is sufficient to unleash the oscillations in the basal
ganglia. This finding allows us to propose a unified explanation for
different phenomena: absence of oscillation in the healthy state of the
basal ganglia, oscillations in dopamine-depleted state and quenching of
oscillations under deep-brain-stimulation (DBS). These novel insights
help us to better understand and optimize the function of DBS protocols.
Furthermore, studying the model behavior under transient increase of
activity of the striatal neurons projecting to the indirect pathway, we
are able to account for both motor impairment in PD patients and for
reduced response inhibition in DBS implanted patients.
Keywords: basal ganglia, Parkinson’s disease, oscillations, deep-brain-stimulation, spiking neural networks
Citation: Kumar A, Cardanobile S, Rotter S and
Aertsen A (2011) The role of inhibition in generating and controlling
Parkinson’s disease oscillations in the basal ganglia. Front. Syst. Neurosci. 5:86. doi: 10.3389/fnsys.2011.00086
Received: 26 May 2011; Accepted: 03 October 2011;
Published online: 24 October 2011.
Edited by:
Raphael Pinaud, University of Oklahoma Health Sciences Center, USA
Copyright: © 2011 Kumar, Cardanobile, Rotter and
Aertsen. This is an open-access article subject to a non-exclusive
license between the authors and Frontiers Media SA, which permits use,
distribution and reproduction in other forums, provided the original
authors and source are credited and other Frontiers conditions are
complied with.
*Correspondence: Ad Aertsen, Department of
Neurobiology and Biophysics, University of Freiburg, D-79104 Freiburg,
Germany. e-mail: aertsen@biologie.uni-freiburg.de