Evidence map›Paper›PMID 23823008›Full record

ArticlePloS one2013

Prolonged Ketamine Effects in Sp4 Hypomorphic Mice: Mimicking Phenotypes of Schizophrenia.

Baohu Ji, Xin Wang, Antonio Pinto-Duarte, Minjung Kim, Sorana Caldwell, Jared W Young, Margarita M Behrens, Terrence J Sejnowski, Mark A Geyer, Xianjin Zhou

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. 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
1.2field-weighted citation impact, top 22% 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, 29 citations in OpenAlex.

  1. Pro-Cognitive Effects of IgM Isotype Anti-NMDAR1 Autoantibodies in Mice.bioRxiv : the preprint server for biology · 2026
    Article
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  6. Review
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  8. Dynamic Communications Between GABAFrontiers in cellular neuroscience · 2018
    Article
  9. Neurophysiological Characterization of Attentional Performance Dysfunction in Schizophrenia Patients in a Reverse-Translated Task.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  10. Article
  11. Article
  12. GlyT-1 Inhibition Attenuates Attentional But Not Learning or Motivational Deficits of the Sp4 Hypomorphic Mouse Model Relevant to Psychiatric Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Article
  13. Article
  14. Transcription factor SP4 phosphorylation is altered in the postmortem cerebellum of bipolar disorder and schizophrenia subjects.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2015
    Article
  15. Article
  16. Article
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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

10 authors at 4 institutions in 2 countries.

Baohu JiDepartment of Psychiatry, University of California San Diego, La Jolla, California, United States of America.
Xin Wang
Antonio Pinto-Duarte
Minjung Kim
Sorana Caldwell
Jared W Young
Margarita M Behrens
Terrence J Sejnowski
Mark A Geyer
Xianjin Zhou
University of California, San Diego · USSalk Institute for Biological Studies · USUniversity of Lisbon · PTVA San Diego Healthcare System · US

Funding

Sp4 Pathway in the Modulation of Sensorimotor Gating and MemoryR01MH073991 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHOU, XIANJIN · 2006 to 2014
$2.9M
Sensitive and Treatable Periods of Brain-Redox Imbalance in SchizophreniaR01MH091407 · NIMH · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI BEHRENS, M MARGARITA, POWELL, SUSAN B · 2010 to 2014
$2.1M
Howard Hughes Medical InstituteNIMH NIH HHS R01 MH073991NIMH NIH HHS R01 MH091407
6 · The paper itself

Abstract

It has been well established that schizophrenia patients display impaired NMDA receptor (NMDAR) functions as well as exacerbation of symptoms in response to NMDAR antagonists. Abnormal NMDAR signaling presumably contributes to cognitive deficits which substantially contribute to functional disability in schizophrenia. Establishing a mouse genetic model will help investigate molecular mechanisms of hypoglutmatergic neurotransmission in schizophrenia. Here, we examined the responses of Sp4 hypomorphic mice to NMDAR antagonists in electroencephalography and various behavioral paradigms. Sp4 hypomorphic mice, previously reported to have reduced NMDAR1 expression and LTP deficit in hippocampal CA1, displayed increased sensitivity and prolonged responses to NMDAR antagonists. Molecular studies demonstrated reduced expression of glutamic acid decarboxylase 67 (GAD67) in both cortex and hippocampus, consistent with abnormal gamma oscillations in Sp4 hypomorphic mice. On the other hand, human SP4 gene was reported to be deleted in schizophrenia. Several human genetic studies suggested the association of SP4 gene with schizophrenia and other psychiatric disorders. Therefore, elucidation of the Sp4 molecular pathway in Sp4 hypomorphic mice may provide novel insights to our understanding of abnormal NMDAR signaling in schizophrenia.

Indexed as

Disease Models, AnimalAnimalsKetamineLong-Term PotentiationMicePhenotypeReceptors, N-Methyl-D-AspartateSchizophreniaSignal TransductionSp4 Transcription FactorKetamineReceptors, N-Methyl-D-AspartateSp4 protein, mouseSp4 Transcription Factor

Identifiers

PMID23823008
PMCPMC3688895
OpenAlexW2061543322

What OpenQuestion holds

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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.