Evidence map›Paper›PMID 31824347›Full record

ReviewFrontiers in psychiatry2019

Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?

Alexei M Bygrave, Kasyoka Kilonzo, Dimitri M Kullmann, David M Bannerman, Dennis Kätzel

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. Article
  7. Potential Roles for the GluN2D NMDA Receptor Subunit in Schizophrenia.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

5 authors at 4 institutions in 3 countries.

Alexei M BygraveDepartment of Neuroscience, Johns Hopkins University, Baltimore, MD, United States.
Kasyoka KilonzoInstitute of Applied Physiology, Ulm University, Ulm, Germany.
Dimitri M KullmannUCL Queen Square Institute of Neurology, University College London, London, United Kingdom.
David M BannermanDepartment of Experimental Psychology, University of Oxford, Oxford, United Kingdom.
Dennis KätzelInstitute of Applied Physiology, Ulm University, Ulm, Germany.
Technische Hochschule Ulm · DEJohns Hopkins University · USNational Hospital for Neurology and Neurosurgery · GBUniversity of Oxford · GB

Funding

Medical Research Council G0400136Medical Research Council G0400627Medical Research Council G0501424Medical Research Council G0600368Medical Research Council G0601440Medical Research Council G0900613Medical Research Council G116/147Medical Research Council G9805989Medical Research Council MR/L01095X/1Wellcome Trust 209807/Z/17/ZWellcome Trust 212285/Z/18/Z
6 · The paper itself

Abstract

Hypofunction of N-methyl-D-aspartate glutamate receptors (NMDARs), whether caused by endogenous factors like auto-antibodies or mutations, or by pharmacological or genetic manipulations, produces a wide variety of deficits which overlap with-but do not precisely match-the symptom spectrum of schizophrenia. In order to understand how NMDAR hypofunction leads to different components of the syndrome, it is necessary to take into account which neuronal subtypes are particularly affected by it in terms of detrimental functional alterations. We provide a comprehensive overview detailing findings in rodent models with cell type-specific knockout of NMDARs. Regarding inhibitory cortical cells, an emerging model suggests that NMDAR hypofunction in parvalbumin (PV) positive interneurons is a potential

Indexed as

catatonic schizophreniaketamineMK-801N-methyl-D-aspartate receptorN-methyl-D-aspartate receptor hypofunctionparvalbuminpsychosisschizophrenia

Identifiers

PMID31824347
PMCPMC6881463
OpenAlexW2981742297

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.