Evidence map›Paper›PMID 28375208›Full record

ArticleTranslational psychiatry2017

Delineation of molecular pathway activities of the chronic antidepressant treatment response suggests important roles for glutamatergic and ubiquitin-proteasome systems.

D I Park, C Dournes, I Sillaber, M Ising, J M Asara, C Webhofer, M D Filiou, M B Müller, C W Turck

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

D I ParkDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
C DournesDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
I SillaberPhenoquest AG, Martinsried, Germany.
M IsingDepartment of Clinical Research, Max Planck Institute of Psychiatry, Munich, Germany.
J M AsaraDivision of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA, USA.
C WebhoferDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
M D FiliouDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
M B MüllerDivision of Experimental Psychiatry, Focus Program Translational Neuroscience, Department of Psychiatry and Psychotherapy, Johannes Gutenberg University Medical Center, Mainz, Germany.
C W TurckDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Max Planck Institute of Psychiatry · DEHarvard University · USJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to identify molecular pathways related to antidepressant response. We administered paroxetine to the DBA/2J mice for 28 days. Following the treatment, the mice were grouped into responders or non-responders depending on the time they spent immobile in the forced swim test. Hippocampal metabolomics and proteomics analyses revealed that chronic paroxetine treatment affects glutamate-related metabolite and protein levels differentially in the two groups. We found significant differences in the expression of N-methyl-d-aspartate receptor and neuronal nitric oxide synthase proteins between the two groups, without any significant alterations in the respective transcript levels. In addition, we found that chronic paroxetine treatment altered the levels of proteins associated with the ubiquitin-proteasome system (UPS). The soluble guanylate cyclase-β1, proteasome subunit α type-2 and ubiquitination levels were also affected in peripheral blood mononuclear cells from antidepressant responder and non-responder patients suffering from major depressive disorder. We submit that the glutamatergic system and UPS have a crucial role in the antidepressant treatment response in both mice and humans.

Indexed as

AnimalsAntidepressive AgentsGlutamic AcidHippocampusHumansLeukocytes, MononuclearMajor Depressive DisorderMaleMetabolomicsMiceMice, Inbred DBANitric Oxide Synthase Type IParoxetineProteasome Endopeptidase ComplexProteomicsReceptors, N-Methyl-D-AspartateAntidepressive AgentsGlutamic AcidNitric Oxide Synthase Type IParoxetineProteasome Endopeptidase ComplexReceptors, N-Methyl-D-AspartateUbiquitin

Identifiers

PMID28375208
PMCPMC5416684
OpenAlexW2604729695

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LicenceCC BY
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Registered trials

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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.