Evidence map›Paper›PMID 26057047›Full record

ArticleTranslational psychiatry2015

Deletion of Rapgef6, a candidate schizophrenia susceptibility gene, disrupts amygdala function in mice.

R J Levy, M Kvajo, Y Li, E Tsvetkov, W Dong, Y Yoshikawa, T Kataoka, V Y Bolshakov, M Karayiorgou, J A Gogos

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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.

R J LevyDepartment of Neuroscience, Columbia University, New York, NY, USA.
M Kvajo1] Department of Physiology and Cellular Biology, Columbia University, New York, NY, USA [2] Department of Psychiatry, Columbia University, New York, NY, USA.
Y LiDepartment of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA.
E TsvetkovDepartment of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA.
W DongDepartment of Otolaryngology, Loma Linda University, Loma Linda, CA, USA.
Y YoshikawaDivision of Molecular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
T KataokaDivision of Molecular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
V Y BolshakovDepartment of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA.
M KarayiorgouDepartment of Psychiatry, Columbia University, New York, NY, USA.
J A Gogos1] Department of Neuroscience, Columbia University, New York, NY, USA [2] Department of Physiology and Cellular Biology, Columbia University, New York, NY, USA.
Columbia University · USHarvard University · USKobe University · JPLoma Linda University · US

Funding

Elucidating the Effect of Disc 1 on Neurodevelopment and Synaptic TransmissionR01MH080234 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOGOS, JOSEPH A · 2007 to 2016
$3.3M
NIMH NIH HHS MH080234NIMH NIH HHS R01 MH080234
6 · The paper itself

Abstract

In human genetic studies of schizophrenia, we uncovered copy-number variants in RAPGEF6 and RAPGEF2 genes. To discern the effects of RAPGEF6 deletion in humans, we investigated the behavior and neural functions of a mouse lacking Rapgef6. Rapgef6 deletion resulted in impaired amygdala function measured as reduced fear conditioning and anxiolysis. Hippocampal-dependent spatial memory and prefrontal cortex-dependent working memory tasks were intact. Neural activation measured by cFOS phosphorylation demonstrated a reduction in hippocampal and amygdala activation after fear conditioning, while neural morphology assessment uncovered reduced spine density and primary dendrite number in pyramidal neurons of the CA3 hippocampal region of knockout mice. Electrophysiological analysis showed enhanced long-term potentiation at cortico-amygdala synapses. Rapgef6 deletion mice were most impaired in hippocampal and amygdalar function, brain regions implicated in schizophrenia pathophysiology. The results provide a deeper understanding of the role of the amygdala in schizophrenia and suggest that RAPGEF6 may be a novel therapeutic target in schizophrenia.

Indexed as

Conditioning, PsychologicalFearAmygdalaAnimalsAnxietyCA3 Region, HippocampalDendritic SpinesDNA Copy Number VariationsGuanine Nucleotide Exchange FactorsHippocampusLong-Term PotentiationMemory, Short-TermMiceMice, KnockoutPhosphorylationPrefrontal CortexGuanine Nucleotide Exchange FactorsProto-Oncogene Proteins c-fosRapgef6 protein, mouse

Identifiers

PMID26057047
PMCPMC4490285
OpenAlexW2122704027

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.