Evidence map›Paper›PMID 34462417›Full record

ArticleTranslational psychiatry2021

Alteration of NMDA receptor trafficking as a cellular hallmark of psychosis.

Agnès Espana, Henrik Seth, Julie Jézéquel, Tingting Huang, Delphine Bouchet, Marylin Lepleux, Hélène Gréa, Karl Bechter, Marion Schneider, Eric Hanse and 1 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Autoimmune neuropsychiatric disorders manifesting with psychosis.The Journal of clinical investigation · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
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  11. Targeting the Limbic System: Insights into Its Involvement in Tinnitus.International journal of molecular sciences · 2023
    Review
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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

11 authors at 4 institutions in 3 countries.

Agnès Espana *Université de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Henrik Seth *Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Goteborg, Gothenburg, Sweden.
Julie JézéquelUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Tingting HuangUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Delphine BouchetUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Marylin LepleuxUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Hélène GréaUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Karl BechterClinic for Psychiatry and Psychotherapy II, Ulm University, Bezirkskrankenhaus Günzburg Ludwig-Heilmeyer-Str. 4, D-89312, Günzburg, Germany.ORCID http://orcid.org/0000-0003-4371-2932
Marion SchneiderDivision of Experimental Anesthesiology, University Hospital Ulm, 89081, Ulm, Germany.
Eric HanseDepartment of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Goteborg, Gothenburg, Sweden.
Laurent GrocUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France. laurent.groc@u-bordeaux.fr.ORCID http://orcid.org/0000-0003-1814-8145
Centre National de la Recherche Scientifique · FRUniversity of Gothenburg · SEUniversität Ulm · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A dysfunction of the glutamatergic transmission, especially of the NMDA receptor (NMDAR), constitutes one of the main biological substrate of psychotic disorders, such as schizophrenia. The NMDAR signaling hypofunction, through genetic and/or environmental insults, would cause a neurodevelopmental myriad of molecular, cellular, and network alterations that persist throughout life. Yet, the mechanisms underpinning NMDAR dysfunctions remain elusive. Here, we compared the membrane trafficking of NMDAR in three gold-standard models of schizophrenia, i.e., patient's cerebrospinal fluids, genetic manipulations of susceptibility genes, and prenatal developmental alterations. Using a combination of single nanoparticle tracking, electrophysiological, biochemical, and behavioral approaches in rodents, we identified that the NMDAR trafficking in hippocampal neurons was consistently altered in all these different models. Artificial manipulations of the NMDAR surface dynamics with competing ligands or antibody-induced receptor cross-link in the developing rat brain were sufficient to regulate the adult acoustic startle reflex and compensate for an early pathological challenge. Collectively, we show that the NMDAR trafficking is markedly altered in all clinically relevant models of psychosis, opening new avenues of therapeutical strategies.

Indexed as

Psychotic DisordersSchizophreniaAnimalsHippocampusRatsReceptors, N-Methyl-D-AspartateSignal TransductionReceptors, N-Methyl-D-Aspartate

Identifiers

PMID34462417
PMCPMC8405679
OpenAlexW3198144325

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.