Emergence of Beta Oscillations of a Resonance Model for Parkinson's Disease

In Parkinson's disease, the excess of beta oscillations in cortical-basal ganglia (BG) circuits has been correlated with normal movement suppression. In this paper, a physiologically based resonance model, generalizing an earlier model of the STN-GPe circuit, is employed to analyze critical dynamics of the occurrence of beta oscillations, which correspond to Hopf bifurcation. With the experimentally measured parameters, conditions for the occurrence of Hopf bifurcation with time delay are deduced by means of linear stability analysis, center manifold theorem, and normal form analysis. It is found that beta oscillations can be induced by increasing synaptic transmission delay. Furthermore, it is revealed that the oscillations originate from interaction among different synaptic connections. Our analytical results are consistent with the previous experimental and simulating findings, thus may provide a more systematic insight into the mechanisms underlying the transient beta bursts.