The possible mechanism of direct feedback projections from basal ganglia to cortex in beta oscillations of Parkinson’s disease: A theoretical evidence in the competing resonance model

Abstract

In this paper, we use a cortex-basal ganglia resonance network to explore the possible Hopf bifurcation mechanism of beta oscillation. Different from traditional viewpoints, this model contains a direct inhibitory projection from the subthalamic nucleus (STN) to the cortex excitatory nuclei (EXN). First, we obtain the oscillation critical conditions of the delay by Hopf bifurcation analysis. Then, we explore the effects of some key parameters on Hopf bifurcation points. Delay is an indispensable factor in this model, oscillations will occur only when delay increases to a certain extent. Interestingly, the amplitude of oscillation increases with an increase in delay, but the trend of frequency is opposite; and heterogeneous delays have different effects on amplitude and frequency. The inhibitory coupling weight in the pathway “STN→EXN” can reduce the firing activation level of cortical circuit, and the increase of coupling weights in the closed loop of the STN and globus pallidus external (GPe) can disinhibition this effect. On the stable boundary curve, the quantitative relationship of coupling weights between the direct and indirect projection from the basal ganglia to cortex is monotonously increasing. An increase in some critical coupling weights in the model, the bidirectional Hopf bifurcations (supercritical and subcritical) occur alternately, which can uniformly explain the origin mechanism of oscillations. In the inhibition-excitation closed loops, the excitatory and inhibitory connection weights have different effects on oscillations, the quantitative relationship of which is monotonically decreasing under Hopf bifurcation critical conditions. In the oscillation region, we observe that the amplitude is the smallest near bifurcation points and gradually increases with the evolution of oscillations. Finally, we find that the direct inhibitory projection from the STN to the EXN is a key pathway for external stimuli to control cortical oscillations. All theoretical analysis results compares well to numerical simulations, we hope that theoretical mechanisms obtained in this paper can inspire experimental research in Parkinson’s disease.