This is an historical archive of the activities of the MRC Anatomical Neuropharmacology Unit (MRC ANU) that operated at the University of Oxford from 1985 until March 2015. The MRC ANU established a reputation for world-leading research on the brain, for training new generations of scientists, and for engaging the general public in neuroscience. The successes of the MRC ANU are now built upon at the MRC Brain Network Dynamics Unit at the University of Oxford.

Beta reactivity, prospective facilitation of executive processing, and its dependence on dopaminergic therapy in Parkinson's disease.

J. Neurosci. 2012;32(29):9909-16. 10.1523/JNEUROSCI.0275-12.2012

Beta reactivity, prospective facilitation of executive processing, and its dependence on dopaminergic therapy in Parkinson's disease.

Oswal A, Litvak V, Sauleau P, Peter Brown
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Abstract:
Oscillatory activity in the beta frequency band has been shown to be modulated during the preparation and execution of voluntary movements at both cortical and subcortical levels. The exaggeration of beta activity in the basal ganglia of patients with Parkinson's disease has heightened interest in this phenomenon. However, the precise function, if any, subserved by modulations in beta activity remains unclear. Here we test the hypothesis that beta reactivity can be dissociated from processing of specific actions and can index the salience of cues with respect to future behavior in a way that might help prospectively prioritize resources. To this end we used an experimental paradigm designed to dissociate salient warning cues from processing of specific motor or cognitive actions. We recorded local field potential activity from the subthalamic nucleus of humans undergoing functional neurosurgery for the treatment of Parkinson's disease, while the same patients were on or off the dopamine prodrug levodopa. In this way we demonstrate that beta reactivity is indeed dependent on the salience of cues with respect to future motor and cognitive action and is promoted by dopamine. The loss of normal beta encoding of saliency may underlie some of the motor and cognitive features of basal ganglia disorders such as Parkinson's disease.