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dc.contributor.author
Scheidegger, Milan
dc.contributor.author
Walter, Martin
dc.contributor.author
Lehmann, Mick
dc.contributor.author
Metzger, Coraline
dc.contributor.author
Grimm, Simone
dc.contributor.author
Boeker, Heinz
dc.contributor.author
Bösiger, Peter
dc.contributor.author
Henning, Anke
dc.contributor.author
Seifritz, Erich
dc.date.accessioned
2018-09-20T09:08:25Z
dc.date.available
2017-06-10T10:10:23Z
dc.date.available
2018-09-20T09:06:23Z
dc.date.available
2018-09-20T09:08:25Z
dc.date.issued
2012-09-24
dc.identifier.issn
1932-6203
dc.identifier.other
10.1371/journal.pone.0044799
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/57319
dc.identifier.doi
10.3929/ethz-b-000057319
dc.description.abstract
Increasing preclinical and clinical evidence underscores the strong and rapid antidepressant properties of the glutamate-modulating NMDA receptor antagonist ketamine. Targeting the glutamatergic system might thus provide a novel molecular strategy for antidepressant treatment. Since glutamate is the most abundant and major excitatory neurotransmitter in the brain, pathophysiological changes in glutamatergic signaling are likely to affect neurobehavioral plasticity, information processing and large-scale changes in functional brain connectivity underlying certain symptoms of major depressive disorder. Using resting state functional magnetic resonance imaging (rsfMRI), the „dorsal nexus “(DN) was recently identified as a bilateral dorsal medial prefrontal cortex region showing dramatically increased depression-associated functional connectivity with large portions of a cognitive control network (CCN), the default mode network (DMN), and a rostral affective network (AN). Hence, Sheline and colleagues (2010) proposed that reducing increased connectivity of the DN might play a critical role in reducing depression symptomatology and thus represent a potential therapy target for affective disorders. Here, using a randomized, placebo-controlled, double-blind, crossover rsfMRI challenge in healthy subjects we demonstrate that ketamine decreases functional connectivity of the DMN to the DN and to the pregenual anterior cingulate (PACC) and medioprefrontal cortex (MPFC) via its representative hub, the posterior cingulate cortex (PCC). These findings in healthy subjects may serve as a model to elucidate potential biomechanisms that are addressed by successful treatment of major depression. This notion is further supported by the temporal overlap of our observation of subacute functional network modulation after 24 hours with the peak of efficacy following an intravenous ketamine administration in treatment-resistant depression.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Public Library of Science
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/3.0/
dc.title
Ketamine Decreases Resting State Functional Network Connectivity in Healthy Subjects: Implications for Antidepressant Drug Action
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 3.0 Unported
ethz.journal.title
PLoS ONE
ethz.journal.volume
7
en_US
ethz.journal.issue
9
en_US
ethz.journal.abbreviated
PLoS ONE
ethz.pages.start
e44799
en_US
ethz.size
9 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.nebis
006206116
ethz.publication.place
Lawrence, KS, USA
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
03656 - Bösiger, Peter
en_US
ethz.leitzahl.certified
03656 - Bösiger, Peter
ethz.date.deposited
2017-06-10T10:10:43Z
ethz.source
ECIT
ethz.identifier.importid
imp59364fe506ae096057
ethz.ecitpid
pub:91833
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-20T16:44:49Z
ethz.rosetta.lastUpdated
2021-02-15T01:49:03Z
ethz.rosetta.versionExported
true
ethz.COinS
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