A model description of beta oscillations in the external globus pallidus

The external globus pallidus (GPe), a subcortical nucleus located in the indirect pathway of the basal ganglia, is widely considered to have tight associations with abnormal beta oscillations (13–30 Hz) observed in Parkinson’s disease (PD). Despite that many mechanisms have been put forward to explain the emergence of these beta oscillations, however, it is still unclear the functional contributions of the GPe, especially, whether the GPe itself can generate beta oscillations. To investigate the role played by the GPe in producing beta oscillations, we employ a well described firing rate model of the GPe neural population. Through extensive simulations, we find that the transmission delay within the GPe–GPe pathway contributes significantly to inducing beta oscillations, and the impacts of the time constant and connection strength of the GPe–GPe pathway on generating beta oscillations are non-negligible. Moreover, the GPe firing patterns can be significantly modulated by the time constant and connection strength of the GPe–GPe pathway, as well as the transmission delay within the GPe–GPe pathway. Interestingly, both increasing and decreasing the transmission delay can push the GPe firing pattern from beta oscillations to other firing patterns, including oscillation and non-oscillation firing patterns. These findings suggest that if the transmission delays within the GPe are at least 9.8 ms, beta oscillations can be produced originally in the GPe neural population, which also may be the origin of PD-related beta oscillations and should be regarded as a promising target for treatments for PD.