Parkinson's disease (PD) is a neurodegenerative disease that is common in the elderly population. The most important pathological change in PD is the degeneration and death of dopaminergic neurons in the substantia nigra of the midbrain, which results in a decrease in the dopamine (DA) content of the striatum. The exact cause of this pathological change is still unknown. Numerous studies have shown that the evolution of PD is associated with abnormal oscillatory activities in the basal ganglia, with different oscillation frequency ranges, such as the typical beta band (13-30 Hz), the alpha band (8-12 Hz), the theta band (4-7 Hz) and the delta band (1-3 Hz). Although some studies have implied that abnormal interactions between the subthalamic nucleus (STN) and globus pallidus (GP) neurons may be a key factor required to induce these oscillations, the relative mechanism is still unclear. The effects of other nerve nuclei in the basal ganglia, such as the striatum, on these oscillations are still unknown. The thalamus and cortex both have close input and output relationships with the basal ganglia, and many previous studies have indicated that they may also exert effects on Parkinson's disease oscillation, but the mechanisms involved are unclear. In this paper, we built a corticothalamic-basal ganglia (CTBG) mean firing-rate model to explore the onset mechanisms of these different oscillation phenomena. We found that, in addition to the STN-GP network, Parkinson's disease oscillations may also be induced by changing the coupling strength and delays in other pathways. Different frequency bands appear in the oscillating region, and various boundary conditions are depicted in parameter diagrams. The onset mechanism is well explained both by the model and by the numerical simulation results. Therefore, this model provides a unifying framework for studying the mechanism of Parkinson's disease oscillations, and we hope that the results obtained in this work can inspire future experimental studies. (C) 2018 Elsevier Ltd. All rights reserved.