期刊
JOURNAL OF NEUROSCIENCE
卷 41, 期 10, 页码 2274-2286出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1591-20.2021
关键词
burst coupling; low beta burst; MPTP; nonhuman primate; Parkinson's disease; temporal dynamics
资金
- NINDS NIH HHS [R37 NS077657, P50 NS098573, R01 NS110613, R01 NS117822, R01 NS058945, R01 NS037019] Funding Source: Medline
Studies have shown increased and longer duration beta burst activity in the subthalamic nucleus (STN) and internal segment of the globus pallidus (GPi) in patients with Parkinson's disease, which may serve as a pathophysiological marker. Additionally, greater synchrony of beta burst activity across different brain regions is observed in Parkinson's disease.
Elevated synchronized oscillatory activity in the beta band has been hypothesized to be a pathophysiological marker of Parkinson's disease (PD). Recent studies have suggested that parkinsonism is closely associated with increased amplitude and duration of beta burst activity in the subthalamic nucleus (STN). How beta burst dynamics are altered from the normal to parkinsonian state across the basal ganglia-thalamocortical (BGTC) motor network, however, remains unclear. In this study, we simultaneously recorded local field potential activity from the STN, internal segment of the globus pallidus (GPi), and primary motor cortex (M1) in three female rhesus macaques, and characterized how beta burst activity changed as the animals transitioned from normal to progressively more severe parkinsonian states. Parkinsonism was associated with an increased incidence of beta bursts with longer duration and higher amplitude in the low beta band (8-20 Hz) in both the STN and GPi, but not in M1. We observed greater concurrence of beta burst activity, however, across all recording sites (M1, STN, and GPi) in PD. The simultaneous presence of low beta burst activity across multiple nodes of the BGTC network that increased with severity of PD motor signs provides compelling evidence in support of the hypothesis that low beta synchronized oscillations play a significant role in the underlying pathophysiology of PD. Given its immersion throughout the motor circuit, we hypothesize that this elevated beta-band activity interferes with spatial-temporal processing of information flow in the BGTC network that contributes to the impairment of motor function in PD.
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