The theoretical mechanism of Parkinson’s oscillation frequency bands: a computational model study

Excessive synchronous oscillation activities appear in the brain is a key pathological feature of Parkinson’s disease, the mechanism of which is still unclear. Although some previous studies indicated that $$\beta$$ oscillation (13–30 Hz) may directly originate in the network composed of the subthalamic nucleus (STN) and external globus pallidus (GPe) neurons, specific onset mechanisms of which are unclear, especially theoretical evidences in numerical simulation are still little. In this paper, we employ a STN–GPe mean-field model to explore the onset mechanism of Parkinson’s oscillation. In addition to $$\beta$$ oscillation, we find that some other common oscillation frequency bands can appear in this network, such as the $$\alpha$$ oscillation band (8–12 Hz), the $$\theta$$ oscillation band (4–7 Hz) and $$\delta$$ oscillation band (1–3 Hz). In addition to the coupling weight between the STN and GPe, the delay is also a critical factor to affect oscillatory activities, which can not be neglected compared to other parameters. Through simulation and analysis, we propose two possible theories may induce the system to transfer from the stable state to the oscillatory state in this model: (1). The oscillation activity can be induced when the firing activation level of the population increases to large enough; (2). In some special cases, the population may stay in the high firing rate stable state and the mean discharge rate of which is too large to induce oscillations, then oscillation activities may be induced as the MD decreases to moderate value. In most situations, the change trends of the MD and oscillation dominant frequency are contrary, which may be an important physiological phenomenon shown in this model. The delays and firing rates were obtained by simulating, which may be verified in the experiment in the future.