ArticlePloS one2012
Potential mechanisms for imperfect synchronization in parkinsonian basal ganglia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- The theoretical mechanism of Parkinson's oscillation frequency bands: a computational model study.Cognitive neurodynamics · 2021Article
- Reducing the Effect of Spurious Phase Variations in Neural Oscillatory Signals.Frontiers in computational neuroscience · 2018Article
- The relative phases of basal ganglia activities dynamically shape effective connectivity in Parkinson's disease.Brain : a journal of neurology · 2015Article
- Control of absence seizures induced by the pathways connected to SRN in corticothalamic system.Cognitive neurodynamics · 2015Article
- Identifying the Basal Ganglia network model markers for medication-induced impulsivity in Parkinson's disease patients.PloS one · 2015Article
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2 authors.
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Abstract
Neural activity in the brain of parkinsonian patients is characterized by the intermittently synchronized oscillatory dynamics. This imperfect synchronization, observed in the beta frequency band, is believed to be related to the hypokinetic motor symptoms of the disorder. Our study explores potential mechanisms behind this intermittent synchrony. We study the response of a bursting pallidal neuron to different patterns of synaptic input from subthalamic nucleus (STN) neuron. We show how external globus pallidus (GPe) neuron is sensitive to the phase of the input from the STN cell and can exhibit intermittent phase-locking with the input in the beta band. The temporal properties of this intermittent phase-locking show similarities to the intermittent synchronization observed in experiments. We also study the synchronization of GPe cells to synaptic input from the STN cell with dependence on the dopamine-modulated parameters. Earlier studies showed how the strengthening of dopamine-modulated coupling may lead to transitions from non-synchronized to partially synchronized dynamics, typical in Parkinson's disease. However, dopamine also affects the cellular properties of neurons. We show how the changes in firing patterns of STN neuron due to the lack of dopamine may lead to transition from a lower to a higher coherent state, roughly matching the synchrony levels observed in basal ganglia in normal and parkinsonian states. The intermittent nature of the neural beta band synchrony in Parkinson's disease is achieved in the model due to the interplay of the timing of STN input to pallidum and pallidal neuronal dynamics, resulting in sensitivity of pallidal output to the phase of the arriving STN input. Thus the mechanism considered here (the change in firing pattern of subthalamic neurons through the dopamine-induced change of membrane properties) may be one of the potential mechanisms responsible for the generation of the intermittent synchronization observed in Parkinson's disease.
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