Abstract
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.
Highlights
Parkinson’s disease (PD) is a movement-related brain disorder that is associated with widespread neurodegeneration within the basal ganglia (BG) [1, 2]
To shed light on the role of corticobasal ganglia circuits in the emergence and stabilization of abnormal beta oscillations in PD condition, here we review the experimentally observed changes of neuronal firing rates and firing patterns as well as local field potential (LFP) recordings within the cortex and each BG nucleus following DA loss. is is of importance since whether or not the abnormal beta oscillations are behind the emergence of motor symptoms, their reduction can induce therapeutic effects both in computational and experimental PD models [21,22,23]
It is important to identify networks that are responsible for the generation and propagation of abnormal beta oscillations within the CBGTC loop
Summary
Parkinson’s disease (PD) is a movement-related brain disorder that is associated with widespread neurodegeneration within the basal ganglia (BG) [1, 2]. Emergence of exaggerated beta band (15–30 Hz) neuronal oscillations in the cortex and different BG nuclei, especially in the STN of animal PD models [10] and PD patients [14], is one of the abnormal functional changes following DA loss. The hyperactivity of STN neurons [15] and motor symptoms of PD [14] are early phenomena in PD condition, experimental findings suggested that the enhancement of abnormal beta oscillations within the BG may not appear in the early stages of PD Rather, they may be correlated with the extent of progressive degeneration of nigral DAergic neurons [16]. We briefly discuss the potential role of other mechanisms, such as synaptic plasticity, in shaping physiological and pathological patterns of neuronal activity and synaptic connectivity in the BG
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