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dc.contributor.authorSpencer, Kevin M.
dc.date.accessioned2011-12-06T19:56:11Z
dc.date.issued2009
dc.identifier.citationSpencer, Kevin M. 2009. The functional consequences of cortical circuit abnormalities on gamma oscillations in schizophrenia: insights from computational modeling. Frontiers in Human Neuroscience 3: 33.en_US
dc.identifier.issn1662-5161en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:5361119
dc.description.abstractSchizophrenia is characterized by cortical circuit abnormalities, which might be reflected in γ-frequency (30–100 Hz) oscillations in the electroencephalogram. Here we used a computational model of cortical circuitry to examine the effects that neural circuit abnormalities might have on γ generation and network excitability. The model network consisted of 1000 leaky integrate-and-fire neurons with realistic connectivity patterns and proportions of neuron types [pyramidal cells (PCs), regular-spiking inhibitory interneurons, and fast-spiking interneurons (FSIs)]. The network produced a γ oscillation when driven by noise input. We simulated reductions in: (1) recurrent excitatory inputs to PCs; (2) both excitatory and inhibitory inputs to PCs; (3) all possible connections between cells; (4) reduced inhibitory output from FSIs; and (5) reduced NMDA input to FSIs. Reducing all types of synaptic connectivity sharply reduced γ power and phase synchrony. Network excitability was reduced when recurrent excitatory connections were deleted, but the network showed disinhibition effects when inhibitory connections were deleted. Reducing FSI output impaired γ generation to a lesser degree than reducing synaptic connectivity, and increased network excitability. Reducing FSI NMDA input also increased network excitability, but increased γ power. The results of this study suggest that a multimodal approach, combining non-invasive neurophysiological and structural measures, might be able to distinguish between different neural circuit abnormalities in schizophrenia patients. Computational modeling may help to bridge the gaps between post-mortem studies, animal models, and experimental data in humans, and facilitate the development of new therapies for schizophrenia and neuropsychiatric disorders in general.en_US
dc.language.isoen_USen_US
dc.publisherFrontiers Research Foundationen_US
dc.relation.isversionofdoi://10.3389/neuro.09.033.2009en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769552/pdf/en_US
dash.licenseLAA
dc.subjectreview articleen_US
dc.titleThe Functional Consequences of Cortical Circuit Abnormalities on Gamma Oscillations in Schizophrenia: Insights from Computational Modelingen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalFrontiers in Human Neuroscienceen_US
dash.depositing.authorSpencer, Kevin M.
dc.date.available2011-12-06T19:56:11Z
dash.affiliation.otherHMS^Psychiatry-BOVAMCen_US
dc.identifier.doi10.3389/neuro.09.033.2009*
dash.contributor.affiliatedSpencer, Kevin


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