dc.date.accessioned | 2020-05-18T18:18:30Z | |
dc.date.available | 2020-05-18T18:18:30Z | |
dc.date.created | 2019-05-08T14:17:20Z | |
dc.date.issued | 2019 | |
dc.identifier.citation | Mäki-Marttunen, Tuomo Krull, Florian Bettella, Francesco Hagen, Espen Næss, Solveig Ness, Torbjørn V Moberget, Torgeir Elvsåshagen, Torbjørn Metzner, Christoph Devor, Anna Edwards, Andrew G. Fyhn, Marianne Djurovic, Srdjan Dale, Anders Andreassen, Ole Andreas Einevoll, Gaute . Alterations in schizophrenia-associated genes can lead to increased power in delta oscillations. Cerebral Cortex. 2019, 29(2), 875-891 | |
dc.identifier.uri | http://hdl.handle.net/10852/75878 | |
dc.description.abstract | Genome-wide association studies have implicated many ion channels in schizophrenia pathophysiology. Although the functions of these channels are relatively well characterized by single-cell studies, the contributions of common variation in these channels to neurophysiological biomarkers and symptoms of schizophrenia remain elusive. Here, using computational modeling, we show that a common biomarker of schizophrenia, namely, an increase in delta-oscillation power, may be a direct consequence of altered expression or kinetics of voltage-gated ion channels or calcium transporters. Our model of a circuit of layer V pyramidal cells highlights multiple types of schizophrenia-related variants that contribute to altered dynamics in the delta-frequency band. Moreover, our model predicts that the same membrane mechanisms that increase the layer V pyramidal cell network gain and response to delta-frequency oscillations may also cause a deficit in a single-cell correlate of the prepulse inhibition, which is a behavioral biomarker highly associated with schizophrenia. | en_US |
dc.language | EN | |
dc.rights | Attribution-NonCommercial 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc/4.0/ | |
dc.title | Alterations in schizophrenia-associated genes can lead to increased power in delta oscillations | en_US |
dc.type | Journal article | en_US |
dc.creator.author | Mäki-Marttunen, Tuomo | |
dc.creator.author | Krull, Florian | |
dc.creator.author | Bettella, Francesco | |
dc.creator.author | Hagen, Espen | |
dc.creator.author | Næss, Solveig | |
dc.creator.author | Ness, Torbjørn V | |
dc.creator.author | Moberget, Torgeir | |
dc.creator.author | Elvsåshagen, Torbjørn | |
dc.creator.author | Metzner, Christoph | |
dc.creator.author | Devor, Anna | |
dc.creator.author | Edwards, Andrew G. | |
dc.creator.author | Fyhn, Marianne | |
dc.creator.author | Djurovic, Srdjan | |
dc.creator.author | Dale, Anders | |
dc.creator.author | Andreassen, Ole Andreas | |
dc.creator.author | Einevoll, Gaute | |
cristin.unitcode | 185,53,10,70 | |
cristin.unitname | NORMENT part UiO | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 2 | |
dc.identifier.cristin | 1696402 | |
dc.identifier.bibliographiccitation | info:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cerebral Cortex&rft.volume=29&rft.spage=875&rft.date=2019 | |
dc.identifier.jtitle | Cerebral Cortex | |
dc.identifier.volume | 29 | |
dc.identifier.issue | 2 | |
dc.identifier.startpage | 875 | |
dc.identifier.endpage | 891 | |
dc.identifier.doi | https://doi.org/10.1093/cercor/bhy291 | |
dc.identifier.urn | URN:NBN:no-78973 | |
dc.type.document | Tidsskriftartikkel | en_US |
dc.type.peerreviewed | Peer reviewed | |
dc.source.issn | 1047-3211 | |
dc.identifier.fulltext | Fulltext https://www.duo.uio.no/bitstream/handle/10852/75878/1/maki-marttunen2019alterations.pdf | |
dc.type.version | PublishedVersion | |