GABA-mediated changes in inter-hemispheric beta frequency activity in early-stage Parkinson’s disease

Autor: Caroline Witton, Ian M. Stanford, Stephen D. Hall, Kim C. Rönnqvist, Craig J. McAllister, Emma J. Prokic, Gavin L. Woodhall, Naoki Yamawaki, A.C. Williams
Rok vydání: 2014
Předmět:
Male
magnetoencephalography
Parkinson's disease
Pyridines
Electroencephalography Phase Synchronization
PSD
power spectral density
Severity of Illness Index
Basal ganglia
Beta Rhythm
beta oscillations
primary motor cortex
GABAA receptor
General Neuroscience
musculoskeletal
neural
and ocular physiology
Motor Cortex
Parkinson Disease
Middle Aged
Subthalamic nucleus
medicine.anatomical_structure
AMC
age-matched control
MRBD
movement-related beta desynchronization
Female
Primary motor cortex
Psychology
psychological phenomena and processes
Motor cortex
medicine.drug
Zolpidem
PMBR
post-movement beta rebound
Neuroscience(all)
Article
medicine
Humans
GABA-A Receptor Agonists
UPDRS
Unified Parkinson’s Disease Rating Scale
PD
Parkinson’s disease
Aged
M1
primary motor cortex
GABAA receptors
medicine.disease
MEG
magnetoencephalography
Receptors
GABA-A
Parkinson’s disease
sense organs
Neuroscience
EMG
electromyography
MRI
magnetic resonance imaging
STN
subthalamic nucleus
Zdroj: Neuroscience
ISSN: 0306-4522
DOI: 10.1016/j.neuroscience.2014.09.037
Popis: Highlights • In PD, contralateral M1 showed greater beta power than ipsilateral M1. • Zolpidem reduced contralateral beta power while ipsilateral power was increased. • This resulted in a hemispheric power ratio that approached parity. • Changes were reflected in pre-movement desynchronization and post-movement rebound. • These changes underlie the symptomatic improvements afforded by zolpidem.
In Parkinson’s disease (PD), elevated beta (15–35 Hz) power in subcortical motor networks is widely believed to promote aspects of PD symptomatology, moreover, a reduction in beta power and coherence accompanies symptomatic improvement following effective treatment with l-DOPA. Previous studies have reported symptomatic improvements that correlate with changes in cortical network activity following GABAA receptor modulation. In this study we have used whole-head magnetoencephalography to characterize neuronal network activity, at rest and during visually cued finger abductions, in unilaterally symptomatic PD and age-matched control participants. Recordings were then repeated following administration of sub-sedative doses of the hypnotic drug zolpidem (0.05 mg/kg), which binds to the benzodiazepine site of the GABAA receptor. A beamforming based ‘virtual electrode’ approach was used to reconstruct oscillatory power in the primary motor cortex (M1), contralateral and ipsilateral to symptom presentation in PD patients or dominant hand in control participants. In PD patients, contralateral M1 showed significantly greater beta power than ipsilateral M1. Following zolpidem administration contralateral beta power was significantly reduced while ipsilateral beta power was significantly increased resulting in a hemispheric power ratio that approached parity. Furthermore, there was highly significant correlation between hemispheric beta power ratio and Unified Parkinson’s Disease Rating Scale (UPDRS). The changes in contralateral and ipsilateral beta power were reflected in pre-movement beta desynchronization and the late post-movement beta rebound. However, the absolute level of movement-related beta desynchronization was not altered. These results show that low-dose zolpidem not only reduces contralateral beta but also increases ipsilateral beta, while rebalancing the dynamic range of M1 network oscillations between the two hemispheres. These changes appear to underlie the symptomatic improvements afforded by low-dose zolpidem.
Databáze: OpenAIRE
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