Evidence map›Paper›PMID 31417356›Full record

ReviewFrontiers in molecular neuroscience2019

NMDAR Hypofunction Animal Models of Schizophrenia.

Gloria Lee, Yi Zhou

Abstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Differential and state-dependent effects of the GluN2A-selective positive allosteric modulator GNE-5729 on executive functions.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  12. Sigma-1 Receptor Activation by Fluvoxamine Ameliorates ER Stress, Synaptic Dysfunction and Behavioral Deficits in a Ketamine Model of Schizophrenia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  13. Observational
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9 more citing papers are in PubMed but not listed here.

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

2 authors.

Gloria LeeDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL, United States.
Yi ZhouDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL, United States.

Funding

Molecular, synaptic and circuit basis for 14-3-3 dysfunction-induced behavioral deficitsR01MH115188 · NIMH · FLORIDA STATE UNIVERSITY · PI ZHOU, YI · 2017 to 2021
$1.9M
NIMH NIH HHS R01 MH115188
6 · The paper itself

Abstract

The N-methyl-d-aspartate receptor (NMDAR) hypofunction hypothesis has been proposed to help understand the etiology and pathophysiology of schizophrenia. This hypothesis was based on early observations that NMDAR antagonists could induce a full range of symptoms of schizophrenia in normal human subjects. Accumulating evidence in humans and animal studies points to NMDAR hypofunctionality as a convergence point for various symptoms of schizophrenia. Here we review animal models of NMDAR hypofunction generated by pharmacological and genetic approaches, and how they relate to the pathophysiology of schizophrenia. In addition, we discuss the limitations of animal models of NMDAR hypofunction and their potential utility for therapeutic applications.

Indexed as

14-3-3 proteinsanimal modelsknockout miceNMDARNMDAR antagonistsNMDAR hypofunctionschizophrenia

Identifiers

PMID31417356
PMCPMC6685005

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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.