LAUSR

Parkinson's disease (PD) is a neurodegenerative brain disorder associated with motor and nonmotor symptoms. Exaggerated beta band (15–30 Hz) neuronal oscillations are widely observed in corticobasal ganglia (BG) circuits during parkinsonism. Abnormal beta oscillations have been linked to motor symptoms of PD, but their exact relationship is poorly understood. Nevertheless, reduction of beta oscillations can induce therapeutic effects in PD patients. While it is widely believed that the external globus pallidus (GPe) and subthalamic nucleus (STN) are jointly responsible for abnormal rhythmogenesis in the parkinsonian BG, the role of other cortico-BG circuits cannot be ignored. To shed light on the origin of abnormal beta oscillations in PD, here we review changes of neuronal activity observed in experimental PD models and discuss how the cortex and different BG nuclei cooperate to generate and stabilize abnormal beta oscillations during parkinsonism. This may provide further insights into the complex relationship between abnormal beta oscillations and motor dysfunction in PD, which is crucial for potential target-specific therapeutic interventions in PD patients.