Beta-Band Resonance and Intrinsic Oscillations in a Biophysically Detailed Model of the Subthalamic Nucleus-Globus Pallidus Network

DC FieldValueLanguage
dc.contributor.authorKoelman, Lucas A.-
dc.contributor.authorLowery, Madeleine M.-
dc.date.accessioned2020-02-13T15:08:46Z-
dc.date.available2020-02-13T15:08:46Z-
dc.date.copyright2019 the Authorsen_US
dc.date.issued2019-11-05-
dc.identifier.citationFrontiers in computational neuroscienceen_US
dc.identifier.issn1662-5188-
dc.identifier.urihttp://hdl.handle.net/10197/11284-
dc.description.abstractIncreased beta-band oscillatory activity in the basal ganglia network is associated with Parkinsonian motor symptoms and is suppressed with medication and deep brain stimulation (DBS). The origins of the beta-band oscillations, however, remains unclear with both intrinsic oscillations arising within the subthalamic nucleus (STN)-external globus pallidus (GPe) network and exogenous beta-activity, originating outside the network, proposed as potential sources of the pathological activity. The aim of this study was to explore the relative contribution of autonomous oscillations and exogenous oscillatory inputs in the generation of pathological oscillatory activity in a biophysically detailed model of the parkinsonian STN-GPe network. The network model accounts for the integration of synaptic currents and their interaction with intrinsic membrane currents in dendritic structures within the STN and GPe. The model was used to investigate the development of beta-band synchrony and bursting within the STN-GPe network by changing the balance of excitation and inhibition in both nuclei, and by adding exogenous oscillatory inputs with varying phase relationships through the hyperdirect cortico-subthalamic and indirect striato-pallidal pathways. The model showed an intrinsic susceptibility to beta-band oscillations that was manifest in weak autonomously generated oscillations within the STN-GPe network and in selective amplification of exogenous beta-band synaptic inputs near the network's endogenous oscillation frequency. The frequency at which this resonance peak occurred was determined by the net level of excitatory drive to the network. Intrinsic or endogenously generated oscillations were too weak to support a pacemaker role for the STN-GPe network, however, they were considerably amplified by sparse cortical beta inputs and were further amplified by striatal beta inputs that promoted anti-phase firing of the cortex and GPe, resulting in maximum transient inhibition of STN neurons. The model elucidates a mechanism of cortical patterning of the STN-GPe network through feedback inhibition whereby intrinsic susceptibility to beta-band oscillations can lead to phase locked spiking under parkinsonian conditions. These results point to resonance of endogenous oscillations with exogenous patterning of the STN-GPe network as a mechanism of pathological synchronization, and a role for the pallido-striatal feedback loop in amplifying beta oscillations.en_US
dc.description.sponsorshipEuropean Commission Horizon 2020en_US
dc.format.mediumElectronic-eCollection-
dc.language.isoenen_US
dc.publisherFrontiers Mediaen_US
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en_US
dc.subjectParkinson's diseaseen_US
dc.subjectBasal gangliaen_US
dc.subjectBeta-band oscillationsen_US
dc.subjectGlobus pallidusen_US
dc.subjectMulti-compartmental neuron modelen_US
dc.subjectSubthalamic nucleusen_US
dc.subjectSynchronizationen_US
dc.titleBeta-Band Resonance and Intrinsic Oscillations in a Biophysically Detailed Model of the Subthalamic Nucleus-Globus Pallidus Networken_US
dc.typeJournal Articleen_US
dc.internal.authorcontactotheraoife.ogorman@ucd.ieen_US
dc.statusPeer revieweden_US
dc.identifier.volume13en_US
dc.citation.otherArticle 77en_US
dc.identifier.doi10.3389/fncom.2019.00077-
dc.neeo.contributorKoelman|Lucas A.|aut|-
dc.neeo.contributorLowery|Madeleine M.|aut|-
dc.date.updated2019-12-12T10:53:21Z-
dc.identifier.grantidERC-2014-CoG-646923-DBSModel-
item.grantfulltextopen-
item.fulltextWith Fulltext-
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