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dc.contributor.authorLee, Shaneen_US
dc.contributor.authorSen, Kamalen_US
dc.contributor.authorKopell, Nancyen_US
dc.date.accessioned2018-08-21T12:18:14Z
dc.date.available2018-08-21T12:18:14Z
dc.date.issued2009-12-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000274229000020&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=6e74115fe3da270499c3d65c9b17d654
dc.identifier.citationLee S, Sen K, Kopell N (2009) Cortical Gamma Rhythms Modulate NMDAR-Mediated Spike Timing Dependent Plasticity in a Biophysical Model. PLoS Comput Biol 5(12): e1000602. https://doi.org/10.1371/journal.pcbi.1000602
dc.identifier.issn1553-734X
dc.identifier.urihttps://hdl.handle.net/2144/30840
dc.description.abstractSpike timing dependent plasticity (STDP) has been observed experimentally in vitro and is a widely studied neural algorithm for synaptic modification. While the functional role of STDP has been investigated extensively, the effect of rhythms on the precise timing of STDP has not been characterized as well. We use a simplified biophysical model of a cortical network that generates pyramidal interneuronal gamma rhythms (PING). Plasticity via STDP is investigated at the excitatory pyramidal cell synapse from a gamma frequency (30–90 Hz) input independent of the network gamma rhythm. The input may represent a corticocortical or an information-specific thalamocortical connection. This synapse is mediated by N-methyl-D-aspartate receptor mediated (NMDAR) currents. For distinct network and input frequencies, the model shows robust frequency regimes of potentiation and depression, providing a mechanism by which responses to certain inputs can potentiate while responses to other inputs depress. For potentiating regimes, the model suggests an optimal amount and duration of plasticity that can occur, which depends on the time course for the decay of the postsynaptic NMDAR current. Prolonging the duration of the input beyond this optimal time results in depression. Inserting pauses in the input can increase the total potentiation. The optimal pause length corresponds to the decay time of the NMDAR current. Thus, STDP in this model provides a mechanism for potentiation and depression depending on input frequency and suggests that the slow NMDAR current decay helps to regulate the optimal amplitude and duration of the plasticity. The optimal pause length is comparable to the time scale of the negative phase of a modulatory theta rhythm, which may pause gamma rhythm spiking. Our pause results may suggest a novel role for this theta rhythm in plasticity. Finally, we discuss our results in the context of auditory thalamocortical plasticity.en_US
dc.description.sponsorshipThis work was funded by National Institute of Deafness and Communication Disorders (NIDCD) Grant 1 RO1 DC-007610 - 01A1 (KS), NIH Training Grants T32 MH020064-07 (SL), T32 MH020064-08 (SL), and NSF DMS-0602204 EMSW21-RTG (NK, SL). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. (1 RO1 DC-007610 - 01A1 - National Institute of Deafness and Communication Disorders (NIDCD); T32 MH020064-07 - NIH; T32 MH020064-08 - NIH; DMS-0602204 EMSW21-RTG - NSF)en_US
dc.languageEnglish
dc.publisherPublic Library of Scienceen_US
dc.relation.ispartofPLOS Computational Biology
dc.relation.isversionofhttps://doi.org/10.1371/journal.pcbi.1000602
dc.rightsCopyright: © 2009 Lee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/
dc.subjectScience & technologyen_US
dc.subjectLife Sciences & Biomedicineen_US
dc.subjectBiochemical research methodsen_US
dc.subjectMathematical & computational biologyen_US
dc.subjectBiochemistry & molecular biologyen_US
dc.subjectVisual cortexen_US
dc.subjectGuinea pigsen_US
dc.subjectAnimalsen_US
dc.subjectAuditory cortexen_US
dc.subjectElectroencephalographyen_US
dc.subjectGlutamineen_US
dc.subjectModels, neurologicalen_US
dc.subjectNeuronal plasticityen_US
dc.subjectReceptors, N-methyl-D-aspartateen_US
dc.subjectGamma rhythmsen_US
dc.subjectBiological sciencesen_US
dc.subjectInformation and computing sciencesen_US
dc.subjectMathematical sciencesen_US
dc.subjectBioinformaticsen_US
dc.titleCortical gamma rhythms modulate NMDAR-mediated spike timing dependent plasticity in a biophysical modelen_US
dc.typeArticleen_US
pubs.elements-sourceweb-of-scienceen_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Arts & Sciencesen_US
pubs.organisational-groupBoston University, College of Arts & Sciences, Department of Mathematics & Statisticsen_US
pubs.organisational-groupBoston University, College of Engineeringen_US
pubs.organisational-groupBoston University, College of Engineering, Department of Biomedical Engineeringen_US
pubs.publication-statusPublisheden_US
dc.identifier.orcid0000-0002-8568-8750 (Kopell, Nancy)


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Copyright: © 2009 Lee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright: © 2009 Lee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.