Evidence map›Paper›PMID 30664624›Full record

ArticleTranslational psychiatry2019

Pyk2 in the amygdala modulates chronic stress sequelae via PSD-95-related micro-structural changes.

Enrica Montalban, Omar Al-Massadi, Anna Sancho-Balsells, Verónica Brito, Benoit de Pins, Jordi Alberch, Silvia Ginés, Jean-Antoine Girault, Albert Giralt

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-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

15 citing papers in PubMed, 32 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 2 institutions in 2 countries.

Enrica MontalbanInserm UMR-S 839, 75005, Paris, France.
Omar Al-MassadiInserm UMR-S 839, 75005, Paris, France.
Anna Sancho-BalsellsDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociencies, Universitat de Barcelona, 08036, Barcelona, Spain.
Verónica BritoDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociencies, Universitat de Barcelona, 08036, Barcelona, Spain.
Benoit de PinsInserm UMR-S 839, 75005, Paris, France.
Jordi AlberchDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociencies, Universitat de Barcelona, 08036, Barcelona, Spain.
Silvia GinésDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociencies, Universitat de Barcelona, 08036, Barcelona, Spain.
Jean-Antoine GiraultInserm UMR-S 839, 75005, Paris, France.
Albert GiraltInserm UMR-S 839, 75005, Paris, France. albertgiralt@ub.edu.
Inserm · FRBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major depressive disorder (MDD) is a common disorder with a variety of symptoms including mood alterations, anhedonia, sleep and appetite disorders, and cognitive disturbances. Stressful life events are among the strongest risk factors for developing MDD. At the cellular level, chronic stress results in the modification of dendritic spine morphology and density. Here, we study the role of Pyk2 in the development of depressive-like symptoms induced by a model of chronic unpredictable mild stress (CUMS). Pyk2 is a non-receptor calcium-dependent protein-tyrosine kinase highly expressed in the forebrain principal neurons and involved in spine structure and density regulation. We show that Pyk2 knockout mice are less affected to anxiety-like and anhedonia-like phenotypes induced by the CUMS paradigm. Using region-specific knockout, we demonstrate that this phenotype is fully recapitulated by selective Pyk2 inactivation in the amygdala. We also show that in the absence of Pyk2 the spine alterations, PSD-95 clustering, and NMDA receptors changes induced by the CUMS paradigm are prevented. Our results reveal a possible role for Pyk2 in the response to stress and in synaptic markers expression and spine density regulation in the amygdala. We suggest that Pyk2 contributes to stress-induced responses through micro-structural changes and that its deficit may contribute to the resilience to chronic stress.

Indexed as

AmygdalaAnimalsBehavior, AnimalDendritic SpinesDisease Models, AnimalDisks Large Homolog 4 ProteinFocal Adhesion Kinase 2Major Depressive DisorderMiceMice, KnockoutReceptors, N-Methyl-D-AspartateStress, PsychologicalDisks Large Homolog 4 ProteinFocal Adhesion Kinase 2Ptk2b protein, mouseReceptors, N-Methyl-D-Aspartate

Identifiers

PMID30664624
PMCPMC6341095
OpenAlexW2916879070

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.