Evidence map›Paper›PMID 24257811›Full record

ReviewJournal of psychopharmacology (Oxford, England)2014

Reviewing the ketamine model for schizophrenia.

Joel Frohlich, John D Van Horn

Abstract readReview
In one paragraph

Review in Journal of psychopharmacology (Oxford, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 2 pooled it
7.5field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 2 syntheses or guidelines pooled it, 309 citations in OpenAlex.

  1. Pooled it
  2. Pre-frontal parvalbumin interneurons in schizophrenia: a meta-analysis of post-mortem studies.Journal of neural transmission (Vienna, Austria : 1996) · 2019
    Pooled it
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  8. Reduced auditory evoked gamma-band response and schizophrenia-like clinical symptoms under subanesthetic ketamine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
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  13. Article
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  16. Review
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  19. Esketamine in depression: putative biomarkers from clinical research.European archives of psychiatry and clinical neuroscience · 2025
    Review
  20. Article

79 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 at 2 institutions in 1 country.

Joel Frohlich1UCLA Center for Autism Research and Treatment (CART), University of California, Los Angeles, CA, USA.
John D Van Horn
University of California, Los Angeles · USUniversity of Southern California · US

Funding

Washington University ConsoritumU54EB005149 · NIBIB · BRIGHAM AND WOMEN'S HOSPITAL · PI KIKINIS, RON · 2004 to 2013
$39.3M
TR&D3: Intrinsic Surface MappingP41EB015922 · NIBIB · UNIVERSITY OF SOUTHERN CALIFORNIA · PI VAN HORN, JOHN DARRELL · 2012 to 2022
$14.1M
Multimodality image-based assessment system for traumatic brain injuryR41NS081792 · NINDS · KITWARE, INC. · PI AYLWARD, STEPHEN R · 2013 to 2014
$297k
NIBIB NIH HHS 2U54EB005149NIBIB NIH HHS P41 EB015922NIBIB NIH HHS U54 EB005149NINDS NIH HHS R41 NS081792NINDS NIH HHS R41NS081792
6 · The paper itself

Abstract

The observation that antagonists of the N-methyl-D-aspartate receptor (NMDAR), such as phencyclidine (PCP) and ketamine, transiently induce symptoms of acute schizophrenia had led to a paradigm shift from dopaminergic to glutamatergic dysfunction in pharmacological models of schizophrenia. The glutamate hypothesis can explain negative and cognitive symptoms of schizophrenia better than the dopamine hypothesis, and has the potential to explain dopamine dysfunction itself. The pharmacological and psychomimetic effects of ketamine, which is safer for human subjects than phencyclidine, are herein reviewed. Ketamine binds to a variety of receptors, but principally acts at the NMDAR, and convergent genetic and molecular evidence point to NMDAR hypofunction in schizophrenia. Furthermore, NMDAR hypofunction can explain connectional and oscillatory abnormalities in schizophrenia in terms of both weakened excitation of inhibitory γ-aminobutyric acidergic (GABAergic) interneurons that synchronize cortical networks and disinhibition of principal cells. Individuals with prenatal NMDAR aberrations might experience the onset of schizophrenia towards the completion of synaptic pruning in adolescence, when network connectivity drops below a critical value. We conclude that ketamine challenge is useful for studying the positive, negative, and cognitive symptoms, dopaminergic and GABAergic dysfunction, age of onset, functional dysconnectivity, and abnormal cortical oscillations observed in acute schizophrenia.

Indexed as

Age of OnsetAnimalsDopaminegamma-Aminobutyric AcidHumansKetaminePhencyclidineReceptors, N-Methyl-D-AspartateSchizophreniaSchizophrenic PsychologyDopaminegamma-Aminobutyric AcidKetaminePhencyclidineReceptors, N-Methyl-D-AspartateglutamateKetamineN-methyl-D-aspartate receptorschizophrenia

Identifiers

PMID24257811
PMCPMC4133098
OpenAlexW2128470552

What OpenQuestion holds

Textmetadata
LicenceTDM
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.