Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex

N. Mallet, A. Pogosyan, A. Sharott, J.L. Csicsvari, J. Bolam, P. Brown, P. Magill, Journal of Neuroscience 28 (2008) 4795–4806.

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Journal Article | Published
Author
Mallet,Nicolas; Pogosyan,Alek; Sharott,Andrew; Csicsvari, Jozsef LIST Austria ; Bolam, John Paul; Brown,Peter; Magill,Peter J
Abstract
In the subthalamic nucleus (STN) of Parkinson's disease (PD) patients, a pronounced synchronization of oscillatory activity at beta frequencies (15-30 Hz) accompanies movement difficulties. Abnormal beta oscillations and motor symptoms are concomitantly and acutely suppressed by dopaminergic therapies, suggesting that these inappropriate rhythms might also emerge acutely from disrupted dopamine transmission. The neural basis of these abnormal beta oscillations is unclear, and how they might compromise information processing, or how they arise, is unknown. Using a 6-hydroxydopamine-lesioned rodent model of PD, we demonstrate that beta oscillations are inappropriately exaggerated, compared with controls, in a brain-state-dependent manner after chronic dopamine loss. Exaggerated beta oscillations are expressed at the levels of single neurons and small neuronal ensembles, and are focally present and spatially distributed within STN. They are also expressed in synchronous population activities, as evinced by oscillatory local field potentials, in STN and cortex. Excessively synchronized beta oscillations reduce the information coding capacity of STN neuronal ensembles, which may contribute to parkinsonian motor impairment. Acute disruption of dopamine transmission in control animals with antagonists of D-1/D-2 receptors did not exaggerate STN or cortical beta oscillations. Moreover, beta oscillations were not exaggerated until several days after 6-hydroxydopamine injections. Thus, contrary to predictions, abnormally amplified beta oscillations in cortico-STN circuits do not result simply from an acute absence of dopamine receptor stimulation, but are instead delayed sequelae of chronic dopamine depletion. Targeting the plastic processes underlying the delayed emergence of pathological beta oscillations after continuing dopaminergic dysfunction may offer considerable therapeutic promise.
Publishing Year
Date Published
2008-04-30
Journal Title
Journal of Neuroscience
Volume
28
Issue
18
Page
4795 - 4806
IST-REx-ID

Cite this

Mallet N, Pogosyan A, Sharott A, et al. Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex. Journal of Neuroscience. 2008;28(18):4795-4806. doi:10.1523/JNEUROSCI.0123-08.2008
Mallet, N., Pogosyan, A., Sharott, A., Csicsvari, J. L., Bolam, J., Brown, P., & Magill, P. (2008). Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex. Journal of Neuroscience, 28(18), 4795–4806. https://doi.org/10.1523/JNEUROSCI.0123-08.2008
Mallet, Nicolas, Alek Pogosyan, Andrew Sharott, Jozsef L Csicsvari, John Bolam, Peter Brown, and Peter Magill. “Disrupted Dopamine Transmission and the Emergence of Exaggerated Beta Oscillations in Subthalamic Nucleus and Cerebral Cortex.” Journal of Neuroscience 28, no. 18 (2008): 4795–4806. https://doi.org/10.1523/JNEUROSCI.0123-08.2008.
N. Mallet et al., “Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex,” Journal of Neuroscience, vol. 28, no. 18, pp. 4795–4806, 2008.
Mallet N, Pogosyan A, Sharott A, Csicsvari JL, Bolam J, Brown P, Magill P. 2008. Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex. Journal of Neuroscience. 28(18), 4795–4806.
Mallet, Nicolas, et al. “Disrupted Dopamine Transmission and the Emergence of Exaggerated Beta Oscillations in Subthalamic Nucleus and Cerebral Cortex.” Journal of Neuroscience, vol. 28, no. 18, Society for Neuroscience, 2008, pp. 4795–806, doi:10.1523/JNEUROSCI.0123-08.2008.

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