Examining Oscillation and Resonance Properties of Feedback Loops Inside  the Basal Ganglia

Investigation under which conditions beta oscillations, as observed in Parkinson's disease, can emerge within the STN-GPe loop, within the STR-GPe loop, or as an interaction between the two loops.

Various hypotheses have been put forth, offering different mechanistic explanations for the emergence of beta oscillations in PD [1]. They can be categorized into three groups of hypotheses that suggest different neural structures to be responsible for the generation of exaggerated beta oscillations:

  1. STN-GPe loop within the basal ganglia,
  2. the striatal microcircuit,
  3. cortical beta oscillations.

According to hypotheses (1) and (2), changes in the dopaminergic innervation of the respective neural structures have been suggested to lead to changes in the neural circuitry that promote beta oscillations. On the other hand, hypothesis (3) suggests that these changes do not generate the beta oscillations by themselves, but rather change the resonance properties of the basal ganglia input structures, leading to an amplification of cortical beta oscillations. In this project, we investigate under which conditions beta oscillations as observed in PD can emerge within the STN-GPe loop, within the STR-GPe loop or as an interaction between the two loops. Furthermore, we characterize the susceptibility to and amplification of cortical stimulation of those circuits. To this end, we apply bifurcation and time-frequency analysis to mean-field models of the dynamic interactions between STN, GPe and STR under conditions of constant or periodic cortical forcing.

[1] Pavlides A, Hogan SJ, Bogacz R.  Computational Models Describing Possible Mechanisms for Generation of excessive Beta Oscillations in Parkinson’s Disease. PLoS Computational Biology. 2015; 11(12).

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