Evidence map›Paper›PMID 26915535›Full record

ArticleHuman brain mapping2016

Ketamine administration reduces amygdalo-hippocampal reactivity to emotional stimulation.

Milan Scheidegger, Anke Henning, Martin Walter, Mick Lehmann, Rainer Kraehenmann, Heinz Boeker, Erich Seifritz, Simone Grimm

Open access · greenAbstract read
In one paragraph

Article in Human brain mapping, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

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  12. Network localization of brain functional effects of ketamine treatment for major depression.European psychiatry : the journal of the Association of European Psychiatrists · 2026
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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

8 authors at 5 institutions in 2 countries.

Milan ScheideggerDepartment of Psychiatry, Psychotherapy and Psychosomatics, Zürich University Hospital for Psychiatry, Switzerland.
Anke HenningInstitute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland.
Martin WalterClinical Affective Neuroimaging Laboratory, Leibniz Institute for Neurobiology, Otto-von-Guericke University, Magdeburg, Germany.
Mick LehmannDepartment of Psychiatry, Psychotherapy and Psychosomatics, Zürich University Hospital for Psychiatry, Switzerland.
Rainer KraehenmannDepartment of Psychiatry, Psychotherapy and Psychosomatics, Zürich University Hospital for Psychiatry, Switzerland.
Heinz BoekerDepartment of Psychiatry, Psychotherapy and Psychosomatics, Zürich University Hospital for Psychiatry, Switzerland.
Erich SeifritzDepartment of Psychiatry, Psychotherapy and Psychosomatics, Zürich University Hospital for Psychiatry, Switzerland.
Simone GrimmDepartment of Psychiatry, Psychotherapy and Psychosomatics, Zürich University Hospital for Psychiatry, Switzerland.
University Hospital of Zurich · CHETH Zurich · CHCharité - Universitätsmedizin 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

Increased amygdala reactivity might lead to negative bias during emotional processing that can be reversed by antidepressant drug treatment. However, little is known on how N-methyl-d-aspartate (NMDA) receptor antagonism with ketamine as a novel antidepressant drug target might modulate amygdala reactivity to emotional stimulation. Using functional magnetic resonance imaging (fMRI) and resting-state fMRI (rsfMRI), we assessed amygdalo-hippocampal reactivity at baseline and during pharmacological stimulation with ketamine (intravenous bolus of 0.12 mg/kg, followed by a continuous infusion of 0.25 mg/kg/h) in 23 healthy subjects that were presented with stimuli from the International Affective Picture System (IAPS). We found that ketamine reduced neural reactivity in the bilateral amygdalo-hippocampal complex during emotional stimulation. Reduced amygdala reactivity to negative pictures was correlated to resting-state connectivity to the pregenual anterior cingulate cortex. Interestingly, subjects experienced intensity of psychedelic alterations of consciousness during ketamine infusion predicted the reduction in neural responsivity to negative but not to positive or neutral stimuli. Our findings suggest that the pharmacological modulation of glutamate-responsive cerebral circuits, which is associated with a shift in emotional bias and a reduction of amygdalo-hippocampal reactivity to emotional stimuli, represents an early biomechanism to restore parts of the disrupted neurobehavioral homeostasis in MDD patients. Hum Brain Mapp 37:1941-1952, 2016. © 2016 Wiley Periodicals, Inc.

Indexed as

AdultAmygdalaAnalysis of VarianceEmotionsExcitatory Amino Acid AntagonistsFemaleHealthy VolunteersHippocampusHumansImage Processing, Computer-AssistedKetamineMagnetic Resonance ImagingMaleOxygenPsychometricsReaction TimeExcitatory Amino Acid AntagonistsKetamineOxygenantidepressantsdepressionemotional processingfMRIglutamateketamine

Identifiers

PMID26915535
PMCPMC6867525
OpenAlexW2279757001

What OpenQuestion holds

Textmetadata
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.