Oscillatory Activity and Synchronization in the Basal Ganglia Network in Rodent Models of Parkinson’s Disease

2009 ◽  
pp. 443-459 ◽  
Author(s):  
Judith R. Walters ◽  
Patrick L. Tierney ◽  
Debra A. Bergstrom
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Oscillatory Activity ◽  
Rodent Models

scholarly journals A dynamical model for the basal ganglia-thalamo-cortical oscillatory activity and its implications in Parkinson’s disease

2020 ◽  
Author(s):  
Eva M. Navarro-López ◽  
Utku Çelikok ◽  
Neslihan S. Şengör
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Activity Patterns ◽  
Dynamical Model ◽  
Substantia Nigra Pars Compacta ◽  
Oscillatory Activity ◽  
Subcortical Structures ◽  
Neuron Models ◽  
Neuronal Patterns

AbstractWe propose to investigate brain electrophysiological alterations associated with Parkinson’s disease through a novel adaptive dynamical model of the network of the basal ganglia, the cortex and the thalamus. The model uniquely unifies the influence of dopamine in the regulation of the activity of all basal ganglia nuclei, the self-organised neuronal interdependent activity of basal ganglia-thalamo-cortical circuits and the generation of subcortical background oscillations. Variations in the amount of dopamine produced in the neurons of the substantia nigra pars compacta are key both in the onset of Parkinson’s disease and in the basal ganglia action selection. We model these dopamine-induced relationships, and Parkinsonian states are interpreted as spontaneous emergent behaviours associated with different rhythms of oscillatory activity patterns of the basal ganglia-thalamo-cortical network. These results are significant because: (1) the neural populations are built upon single-neuron models that have been robustly designed to have eletrophysiologically-realistic responses, and (2) our model distinctively links changes in the oscillatory activity in subcortical structures, dopamine levels in the basal ganglia and pathological synchronisation neuronal patterns compatible with Parkinsonian states, this still remains an open problem and is crucial to better understand the progression of the disease.

scholarly journals Oscillatory activity in basal ganglia and motor cortex in an awake behaving rodent model of Parkinson's disease

Basal Ganglia ◽  
2014 ◽  
Vol 3 (4) ◽  
pp. 221-227 ◽  
Author(s):  
Claire Delaville ◽  
Ana V. Cruz ◽  
Alex J. McCoy ◽  
Elena Brazhnik ◽  
Irene Avila ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Motor Cortex ◽  
Rodent Model ◽  
Oscillatory Activity

14 Pathological oscillatory activity in Parkinson’s disease; what does it mean and how should we treat it?

2020 ◽  
Vol 91 (8) ◽  
pp. e6.1-e6
Author(s):  
Peter Brown
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Side Effects ◽  
Brain Stimulation ◽  
Neural Circuit ◽  
Symptom Control ◽  
Oscillatory Activity ◽  
Deep Brain

Professor Peter Brown is Professor of Experimental Neurology and Director of the Medical Research Council Brain Network Dynamics Unit at the University of Oxford. Prior to 2010 he was a Professor of Neurology at University College London.For decades we have had cardiac pacemakers that adjust their pacing according to demand and yet therapeutic adaptive stimulation approaches for the central nervous system are still not clinically available. Instead, to treat patients with advanced Parkinson’s disease we stimulate the basal ganglia with fixed regimes, unvarying in frequency or intensity. Although effective, this comes with side-effects and in terms of sophistication this treatment approach could be compared to having central heating system on all the time, regardless of temperature. This talk will describe recent steps being taken to define the underlying circuit dysfunction in Parkinson’s and to improve deep brain stimulation by controlling its delivery according to the state of pathological activity.Evidence is growing that motor symptoms in Parkinson’s disease are due, at least in part, to excessive synchronisation between oscillating neurons. Recordings confirm bursts of oscillatory synchronisation in the basal ganglia centred around 20 Hz. The bursts of 20 Hz activity are prolonged in patients withdrawn from their usual medication and the dominance of these long duration bursts negatively correlates with motor impairment. Longer bursts attain higher amplitudes, indicative of more pervasive oscillatory synchronisation within the neural circuit. In contrast, in heathy primates and in treated Parkinson’s disease bursts tend to be short. Accordingly, it might be best to use closed-loop controlled deep brain stimulation to selectively terminate longer, bigger, pathological beta bursts to both save power and to spare the ability of underlying neural circuits to engage in more physiological processing between long bursts. It is now possible to record and characterise bursts on-line during stimulation of the same site and trial adaptive stimulation. Thus far, this has demonstrated improvements in efficiency and side-effects over conventional continuous stimulation, with at least as good symptom control in Parkinsonian patients.

Slow Brain Potential and Oscillatory EEG Manifestations of Impaired Temporal Preparation in Parkinson's Disease

2007 ◽  
Vol 98 (5) ◽  
pp. 2848-2857 ◽  
Author(s):  
Peter Praamstra ◽  
Paul Pope
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Temporal Structure ◽  
Oscillatory Activity ◽  
Brain Potentials ◽  
Brain Potential ◽  
Temporal Preparation ◽  
Implicit Timing ◽  
Slow Brain Potentials

Performance in behavioral tasks is influenced by temporal expectations shaped by the temporal structure of the task. Such implicit temporal preparation is reflected in slow brain potentials and electroencephalographic oscillations and is attributed to interval timing mechanisms that probably depend on intact basal ganglia function. We investigated implicit timing in Parkinson's disease using a choice reaction task with two temporally regular stimulus presentation regimes, both including occasional deviant interstimulus intervals. Control subjects, but not patients, demonstrated temporal preparation in the form of an adjustment in time course of slow brain potentials to the duration of the interstimulus interval. However, in both groups, timing perturbations were accompanied by a slow brain potential amplitude drop at the time of expected stimulus occurrence, demonstrating intact representation of time in patients. In patients, oscillatory activity in beta and alpha bands showed attenuated preparatory desynchronization and reduced postmovement event-related synchronization, reflecting abnormal engagement and disengagement of sensorimotor and parietal areas. The results demonstrate profoundly deficient temporal preparation with preserved encoding of temporal information, a dissociation that may be explained by impaired dopamine-dependent motor learning. The results are discussed in the context of recent work on oscillatory activity in the basal ganglia.

scholarly journals Hypersynchrony despite pathologically reduced beta oscillations in patients with Parkinson's disease: a pharmaco-magnetoencephalography study

2014 ◽  
Vol 112 (7) ◽  
pp. 1739-1747 ◽  
Author(s):  
Elizabeth Heinrichs-Graham ◽  
Max J. Kurz ◽  
Katherine M. Becker ◽  
Pamela M. Santamaria ◽  
Howard E. Gendelman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Subthalamic Nucleus ◽  
Neurodegenerative Disorder ◽  
Oscillatory Activity ◽  
Cortical Motor ◽  
Motor Network ◽  
Neurophysiological Studies ◽  
Gait Abnormalities

Parkinson's disease (PD) is a progressive debilitating neurodegenerative disorder clinically manifest by motor, posture and gait abnormalities. Human neurophysiological studies recording local field potentials within the subthalamic nucleus and scalp-based electroencephalography have shown pathological beta synchrony throughout the basal ganglia-thalamic-cortical motor network in PD. Notably, suppression of this pathological beta synchrony by dopamine replacement therapy or deep-brain stimulation has been associated with improved motor function. However, due to the invasive nature of these studies, it remains unknown whether this “pathological beta” is actually stronger than that observed in healthy demographically matched controls. We used magnetoencephalography to investigate neuronal synchrony and oscillatory amplitude in the beta range and lower frequencies during the resting state in patients with PD and a matched group of patients without neurological disease. Patients with PD were studied both in the practically defined drug “OFF” state, and after administration of dopamine replacements. We found that beta oscillatory amplitude was reduced bilaterally in the primary motor regions of unmedicated patients with PD compared with controls. Administration of dopaminergic medications significantly increased beta oscillatory activity, thus having a normalizing effect. Interestingly, we also found significantly stronger beta synchrony (i.e., hypersynchrony) between the primary motor regions in unmedicated patients with PD compared with controls, and that medication reduced this coupling which is in agreement with the intraoperative studies. These results are consistent with the known functionality of the basal ganglia-thalamic-cortical motor circuit and the likely consequences of beta hypersynchrony in the subthalamic nucleus of patients with PD.

scholarly journals Parkinsonism and vigilance: alteration in neural oscillatory activity and phase-amplitude coupling in the basal ganglia and motor cortex

2017 ◽  
Vol 118 (5) ◽  
pp. 2654-2669 ◽  
Author(s):  
David Escobar Sanabria ◽  
Luke A. Johnson ◽  
Shane D. Nebeck ◽  
Jianyu Zhang ◽  
Matthew D. Johnson ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Neural Activity ◽  
High Frequency ◽  
Closed Loop ◽  
Oscillatory Activity ◽  
Motor Circuit ◽  
Phase Amplitude ◽  
Frequency Power

Oscillatory neural activity in different frequency bands and phase-amplitude coupling (PAC) are hypothesized to be biomarkers of Parkinson’s disease (PD) that could explain dysfunction in the motor circuit and be used for closed-loop deep brain stimulation (DBS). How these putative biomarkers change from the normal to the parkinsonian state across nodes in the motor circuit and within the same subject, however, remains unknown. In this study, we characterized how parkinsonism and vigilance altered oscillatory activity and PAC within the primary motor cortex (M1), subthalamic nucleus (STN), and globus pallidus (GP) in two nonhuman primates. Static and dynamic analyses of local field potential (LFP) recordings indicate that 1) after induction of parkinsonism using the neurotoxin MPTP, low-frequency power (8–30 Hz) increased in the STN and GP in both subjects, but increased in M1 in only one subject; 2) high-frequency power (~330 Hz) was present in the STN in both normal subjects but absent in the parkinsonian condition; 3) elevated PAC measurements emerged in the parkinsonian condition in both animals, but in different sites in each animal (M1 in one subject and GPe in the other); and 4) the state of vigilance significantly impacted how oscillatory activity and PAC were expressed in the motor circuit. These results support the hypothesis that changes in low- and high-frequency oscillatory activity and PAC are features of parkinsonian pathophysiology and provide evidence that closed-loop DBS systems based on these biomarkers may require subject-specific configurations as well as adaptation to changes in vigilance. NEW & NOTEWORTHY Chronically implanted electrodes were used to record neural activity across multiple nodes in the basal ganglia-thalamocortical circuit simultaneously in a nonhuman primate model of Parkinson’s disease, enabling within-subject comparisons of electrophysiological biomarkers between normal and parkinsonian conditions and different vigilance states. This study improves our understanding of the role of oscillatory activity and phase-amplitude coupling in the pathophysiology of Parkinson’s disease and supports the development of more effective DBS therapies based on pathophysiological biomarkers.

Neuronal beta band oscillatory activity in the basal ganglia reflecting rigidity in Parkinson’s disease patients

2017 ◽  
Vol 381 ◽  
pp. 493
Author(s):  
H. Iwamuro ◽  
Y. Shimo ◽  
A. Umemura ◽  
A. Nakajima ◽  
G. Oyama ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Oscillatory Activity ◽  
Beta Band
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