Abstract
Βeta oscillatory activity (human: 13–35 Hz; primate: 8–24 Hz) is pervasive within the cortex and basal ganglia. Studies in Parkinson’s disease patients and animal models suggest that beta-power increases with dopamine depletion. However, the exact relationship between oscillatory power, frequency and dopamine tone remains unclear. We recorded neural activity in the cortex and basal ganglia of healthy non-human primates while acutely and chronically up- and down-modulating dopamine levels. We assessed changes in beta oscillations in patients with Parkinson’s following acute and chronic changes in dopamine tone. Here we show beta oscillation frequency is strongly coupled with dopamine tone in both monkeys and humans. Power, coherence between single-units and local field potentials (LFP), spike-LFP phase-locking, and phase-amplitude coupling are not systematically regulated by dopamine levels. These results demonstrate that beta frequency is a key property of pathological oscillations in cortical and basal ganglia networks.
Highlights
Βeta oscillatory activity is pervasive within the cortex and basal ganglia
We examined single-unit activity (SUA) and local field potentials (LFP) recordings collected with multiple micro-electrodes from the dorsolateral prefrontal cortex, and the external segment of the globus pallidus (GPe), the central nucleus of basal ganglia (BG) circuitry[5] in awake, behaving monkeys under acute up- and down-modulation of dopamine tone (Fig. 1a–d and Table-S1)[20]
We examined LFP and SUA recordings from the subthalamic nucleus (STN), a BG input nucleus, from monkeys pre- and post-chronic dopamine-denervation via MPTP injection regimen (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) (Fig. 1e–g and Table-S1)
Summary
Βeta oscillatory activity (human: 13–35 Hz; primate: 8–24 Hz) is pervasive within the cortex and basal ganglia. Coherence between single-units and local field potentials (LFP), spike-LFP phase-locking, and phase-amplitude coupling are not systematically regulated by dopamine levels These results demonstrate that beta frequency is a key property of pathological oscillations in cortical and basal ganglia networks. Both were alleviated by dopamine-replacement therapy (DRT) or deep brain stimulation (DBS)[10,12,17,18,19] Based on these studies of beta activity in PD patients and animal models, dopamine is thought to play an important role in modulating the power of beta signaling in CBG networks. Because most of this evidence was derived from dopamine-depleted PD patients and animals models we cannot reliably assume that what we gleaned from these studies provides us with a comprehensive depiction of interactions between dopamine tone and beta oscillation properties, including power, frequency, coherence and single-unit entrainment. We further propose that progressive beta-frequency decline, and not a beta-power amplitude, could be used as a more effective indicator of PD progression and as a trigger for adaptive DBS procedures
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