A study of bidirectional control of Parkinson's beta oscillations by basal ganglia

In this study, we investigate the origin and control mechanism of excessive beta oscillations in the electroencephalogram, a marker of Parkinson's disease (PD). We construct four thalamus-cortex-basal ganglia circuit (TCBGC) computational models to address this. Our analysis reveals that variations in coupling weights within the thalamic circuit can induce beta oscillations through supercritical and subcritical Hopf bifurcations. Beta oscillation frequency and amplitude display contrasting trends across different parameter regions. Modulating the activation level of globus pallidus internal (GPi) can inhibit beta oscillations via projections to specific relay nuclei (SRN) or thalamic reticular nucleus (TRN), suggesting a bidirectional regulatory mechanism. Similarly, globus pallidus externa (GPe) exerts a bidirectional inhibitory effect on beta oscillations. Pathological parameters influence this regulation by shifting Hopf bifurcation points. The cortex exhibits a low critical average discharge rate, whereas GPi and GPe show varying triggering average discharge rates. Both external constant voltage and deep brain stimulation (DBS) effectively suppress beta oscillations by modulating GPi and GPe. Our findings highlight GPi and GPe as potential DBS targets for PD treatment, providing insights into beta oscillation regulation. This work extends previous efforts by exploring beta oscillation dynamics within the TCBGC.