Abstract
Hypokinetic symptoms of Parkinson's disease are usually associated with excessively strong oscillations and synchrony in the beta frequency band. The origin of this synchronized oscillatory dynamics is being debated. Cortical circuits may be a critical source of excessive beta in Parkinson's disease. However, subthalamo-pallidal circuits were also suggested to be a substantial component in generation and/or maintenance of Parkinsonian beta activity. Here we study how the subthalamo-pallidal circuits interact with input signals in the beta frequency band, representing cortical input. We use conductance-based models of the subthalamo-pallidal network and two types of input signals: artificially-generated inputs and input signals obtained from recordings in Parkinsonian patients. The resulting model network dynamics is compared with the dynamics of the experimental recordings from patient's basal ganglia. Our results indicate that the subthalamo-pallidal model network exhibits multiple resonances in response to inputs in the beta band. For a relatively broad range of network parameters, there is always a certain input strength, which will induce patterns of synchrony similar to the experimentally observed ones. This ability of the subthalamo-pallidal network to exhibit realistic patterns of synchronous oscillatory activity under broad conditions may indicate that these basal ganglia circuits are directly involved in the expression of Parkinsonian synchronized beta oscillations. Thus, Parkinsonian synchronized beta oscillations may be promoted by the simultaneous action of both cortical (or some other) and subthalamo-pallidal network mechanisms. Hence, these mechanisms are not necessarily mutually exclusive.
Highlights
Hypokinetic symptoms of Parkinson’s disease are usually associated with excessively strong oscillations and synchrony in the beta frequency range
The parameter Iapp regulates the excitability of GPe model neurons. Lowering this parameter would correspond to stronger striatal inhibition (GPe neuron will exhibit less of its own dynamics and will be more controlled by excitatory inputs from subthalamic nucleus (STN))
We studied the dynamics of subthalamo-pallidal model network under the influence of an input signal derived from recordings made in a patient with Parkinson’s disease
Summary
Hypokinetic symptoms of Parkinson’s disease are usually associated with excessively strong oscillations and synchrony in the beta frequency range (reviewed in, e.g., Hammond et al, 2007; Eusebio and Brown, 2009; Stein and Bar-Gad, 2013). Both cortical and subcortical (basal ganglia) areas express these excessive synchronous oscillatory dynamics. Synchronized Beta-Band Oscillations of this synchrony is affected by dopaminergic status (e.g., Sharott et al, 2005; Mallet et al, 2008a; Hirschmann et al, 2013) emphasizing its relevance to hypokinetic motor symptoms in Parkinson’s disease The origin of this beta-band oscillatory dynamics is being debated. The subthalamo-pallidal circuitry was found to be capable of generation of very realistic oscillatory synchronized patterns of neural activity (Park et al, 2011)
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