A dynamical model of the basal ganglia (Leblois et al 2006)

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Accession:64255
We propose a new model for the function and dysfunction of the basal ganglia (BG). The basal ganglia are a set of cerebral structures involved in motor control which dysfunction causes high-incidence pathologies such as Parkinson's disease (PD). Their precise motor functions remain unknown. The classical model of the BG that allowed for the discovery of new treatments for PD seems today outdated in several respects. Based on experimental observations, our model proposes a simple dynamical framework for the understanding of how BG may select motor programs to be executed. Moreover, we explain how this ability is lost and how tremor-related oscillations in neuronal activity may emerge in PD.
Reference:
1 . Leblois A, Boraud T, Meissner W, Bergman H, Hansel D (2006) Competition between feedback loops underlies normal and pathological dynamics in the basal ganglia J Neurosci 26(13):3567-3583 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Connectionist Network;
Brain Region(s)/Organism: Basal ganglia;
Cell Type(s):
Channel(s):
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: C or C++ program;
Model Concept(s): Oscillations; Spatio-temporal Activity Patterns; Simplified Models; Pathophysiology; Rate-coding model neurons; Parkinson's;
Implementer(s): Leblois, Arthur [leblois at clipper.ens.fr];
  
This is the readme for the model code associated with the paper:

Leblois A, Boraud T, Meissner W, Bergman H, Hansel D (2006)
Competition between Feedback Loops Underlies Pathological Dynamics in
the Basal Ganglia 
J Neurosci 26(13):3567-3583

Abstract:

Experiments performed in normal animals suggest that the basal ganglia
(BG) are crucial in motor program selection. BG are also involved in
movement disorders. In particular, BG neuronal activity in
parkinsonian animals and patients is more oscillatory and more
synchronous than in normal individuals. We propose a new model for the
function and dysfunction of the motor part of BG. We hypothesize that
the striatum, the subthalamic nucleus, the internal pallidum (GPi),
the thalamus, and the cortex are involved in closed feedback
loops. The direct (cortex-striatum-GPi-thalamus-cortex) and the
hyperdirect loops (cortex-subthalamic nucleus-GPi-thalamus-cortex),
which have different polarities, play a key role in the model. We show
that the competition between these two loops provides the BG-cortex
system with the ability to perform motor program selection. Under the
assumption that dopamine potentiates corticostriatal synaptic
transmission, we demonstrate that, in our model, moderate dopamine
depletion leads to a complete loss of action selection ability. High
depletion can lead to synchronous oscillations. These modifications of
the network dynamical state stem from an imbalance between the
feedback in the direct and hyperdirect loops when dopamine is
depleted. Our model predicts that the loss of selection ability occurs
before the appearance of oscillations, suggesting that Parkinson's
disease motor impairments are not directly related to abnormal
oscillatory activity. Another major prediction of our model is that
synchronous oscillations driven by the hyperdirect loop appear in BG
after inactivation of the striatum.

To build the model under linux, download and extract the archive.
"cd" to the code directory and type "make".  Then type "./simulation"
The model in it's default setting will start up.  The model is written
in ANSI C and should work with every C compiler.


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