Evidence map›Paper›PMID 23049758›Full record

Trial reportPloS one2012

Ketamine decreases resting state functional network connectivity in healthy subjects: implications for antidepressant drug action.

Milan Scheidegger, Martin Walter, Mick Lehmann, Coraline Metzger, Simone Grimm, Heinz Boeker, Peter Boesiger, Anke Henning, Erich Seifritz

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 3 pooled it
10.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

140 citing papers in PubMed, 3 syntheses or guidelines pooled it, 276 citations in OpenAlex.

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  10. MDMA-induced changes in within-network connectivity contradict the specificity of these alterations for the effects of serotonergic hallucinogens.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
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  11. Short-term nicotine deprivation alters dorsal anterior cingulate glutamate concentration and concomitant cingulate-cortical functional connectivity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
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  13. Default mode network connectivity change corresponds to ketamine's delayed glutamatergic effects.European archives of psychiatry and clinical neuroscience · 2020
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80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 2 countries.

Milan ScheideggerInstitute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland. scheidegger@biomed.ee.ethz.ch
Martin Walter
Mick Lehmann
Coraline Metzger
Simone Grimm
Heinz Boeker
Peter Boesiger
Anke Henning
Erich Seifritz
ETH Zurich · CHInstitute for Biomedical Engineering · CHCenter for Behavioral Brain Sciences · DEFreie Universität Berlin · DEOtto-von-Guericke University Magdeburg · DESwiss Integrative Center for Human Health · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AdultAntidepressive AgentsBrain MappingCross-Over StudiesDouble-Blind MethodFemaleGyrus CinguliHumansInjections, IntravenousKetamineMagnetic Resonance ImagingMajor Depressive DisorderMaleMiddle AgedNeural PathwaysPlacebosAntidepressive AgentsKetaminePlacebos

Identifiers

PMID23049758
PMCPMC3461985
OpenAlexW1964807622

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.