Generating mechanism of pathological beta oscillations in STN–GPe circuit model: A bifurcation study**Project supported by the National Natural Science Foundation of China (Grant Nos. 61473208 and 61876132) and the Tianjin Research Program of Application Foundation and Advanced Technology, China (Grant No. 15JCYBJC47700).

Abstract

Parkinson’s disease (PD) is characterized by pathological spontaneous beta oscillations (13 Hz–35 Hz) often observed in basal ganglia (BG) composed of subthalamic nucleus (STN) and globus pallidus (GPe) populations. From the viewpoint of dynamics, the spontaneous oscillations are related to limit cycle oscillations in a nonlinear system; here we employ the bifurcation analysis method to elucidate the generating mechanism of the pathological spontaneous beta oscillations underlined by coupling strengths and intrinsic properties of the STN–GPe circuit model. The results reveal that the increase of inter-coupling strength between STN and GPe populations induces the beta oscillations to be generated spontaneously, and causes the oscillation frequency to decrease. However, the increase of intra-coupling (self-feedback) strength of GPe can prevent the model from generating the oscillations, and dramatically increase the oscillation frequency. We further provide a theoretical explanation for the role played by the inter-coupling strength of GPe population in the generation and regulation of the oscillations. Furthermore, our study reveals that the intra-coupling strength of the GPe population provides a switching mechanism on the generation of the abnormal beta oscillations: for small value of the intra-coupling strength, STN population plays a dominant role in inducing the beta oscillations; while for its large value, the GPe population mainly determines the generation of this oscillation.