Evidence map›Paper›PMID 34899420›Full record

ArticleFrontiers in psychiatry2021

Cre-Activation in ErbB4-Positive Neurons of Floxed

Anne S Mallien, Natascha Pfeiffer, Miriam A Vogt, Sabine Chourbaji, Rolf Sprengel, Peter Gass, Dragos Inta

Open access · goldAbstract read
In one paragraph

Article in Frontiers in psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 54% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Future Perspectives of NMDAR in CNS Disorders.Molecules (Basel, Switzerland) · 2025
    Review
  2. Parvalbumin interneuron deficits in schizophrenia.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2024
    Review
  3. Review
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

7 authors at 5 institutions in 2 countries.

Anne S MallienDepartment of Psychiatry and Psychotherapy, Medical Faculty Mannheim, RG Animal Models in Psychiatry, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany.
Natascha PfeifferDepartment of Psychiatry and Psychotherapy, Medical Faculty Mannheim, RG Animal Models in Psychiatry, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany.
Miriam A VogtInterfaculty Biomedical Research Facility (IBF), Heidelberg University, Heidelberg, Germany.
Sabine ChourbajiInterfaculty Biomedical Research Facility (IBF), Heidelberg University, Heidelberg, Germany.
Rolf SprengelResearch Group of the Max Planck Institute for Medical Research at the Institute for Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany.
Peter GassDepartment of Psychiatry and Psychotherapy, Medical Faculty Mannheim, RG Animal Models in Psychiatry, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany.
Dragos IntaDepartment of Psychiatry and Psychotherapy, Medical Faculty Mannheim, RG Animal Models in Psychiatry, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany.
Heidelberg University · DECentral Institute of Mental Health · DEMax Planck Institute for Medical Research · DEUniversity Hospital Heidelberg · DEUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extensive evidence suggests a dysfunction of the glutamate NMDA receptor (NMDAR) in schizophrenia, a severe psychiatric disorder with putative early neurodevelopmental origins, but clinical onset mainly during late adolescence. On the other hand, pharmacological models using NMDAR antagonists and the clinical manifestation of anti-NMDAR encephalitis indicate that NMDAR blockade/hypofunction can trigger psychosis also at adult stages, without any early developmental dysfunction. Previous genetic models of NMDAR hypofunction restricted to parvalbumin-positive interneurons indicate the necessity of an early postnatal impairment to trigger schizophrenia-like abnormalities, whereas the cellular substrates of NMDAR-mediated psychosis at adolescent/adult stages are unknown. Neuregulin 1 (NRG1) and its receptor ErbB4 represent schizophrenia-associated susceptibility factors that closely interact with NMDAR. To determine the neuronal populations implicated in "late" NMDAR-driven psychosis, we analyzed the effect of the inducible ablation of NMDARs in

Indexed as

glutamateneuregulin-1neurodevelopmentNMDA receptorpharmacogeneticpost-adolescentschizophrenia

Identifiers

PMID34899420
PMCPMC8660629
OpenAlexW3215634446

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.