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Acute In Vivo Electrophysiological Recordings of Local Field Potentials and Multi-unit Activity from the Hyperdirect Pathway in Anesthetized Rats
Published on: June 22, 2017
Alterations in brain connectivity underlying beta oscillations in Parkinsonism
Rosalyn J Moran1, Nicolas Mallet, Vladimir Litvak
1Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, United Kingdom. r.moran@fil.ion.ucl.ac.uk
Plos Computational Biology
|August 20, 2011
Summary
Parkinson's disease disrupts brain circuits, causing exaggerated beta oscillations. This study reveals altered connectivity in the cortico-basal ganglia-thalamocortical pathway, highlighting a balance between disease processes and compensation.
Area of Science:
- Neuroscience
- Systems Neuroscience
- Computational Neuroscience
Background:
- Parkinson's disease (PD) involves dopamine depletion, severely disrupting cortico-basal ganglia-thalamocortical circuits.
- This disruption leads to exaggerated beta oscillations (10-35 Hz), which correlate with motor impairments but whose neural basis is unclear.
Purpose of the Study:
- To investigate the effective connectivity changes within the cortico-basal ganglia-thalamocortical circuit in a rat model of PD.
- To understand the neural basis of abnormal beta oscillations and distinguish between pathogenic and compensatory mechanisms.
Main Methods:
- Utilized dynamic causal modelling (DCM) on a 6-hydroxydopamine-lesioned rat model of PD.
- Recorded local field potentials simultaneously from the frontal cortex, striatum, external globus pallidus (GPe), and subthalamic nucleus (STN).
- Analyzed auto-spectral and cross-spectral measures of beta oscillations to optimize neurobiologically plausible models of circuit connectivity.
Main Results:
- Dopamine depletion reorganised the circuit, increasing effective connectivity from the cortex to the subthalamic nucleus (STN).
- Effective connectivity from the STN to the external globus pallidus (GPe) was decreased.
- Contribution analysis revealed that the indirect pathway gained strategic importance, underpinning the excessive beta oscillations observed in PD.
Conclusions:
- Altered effective connectivity in basal ganglia-thalamocortical circuits in PD reflects a balance between pathogenic processes and compensation.
- Findings provide a novel perspective on the neural basis of exaggerated beta synchrony in Parkinson's disease.
- Identified potential new therapeutic targets for addressing dysfunctional oscillations in PD.
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