Evidence map›Paper›PMID 25432637›Full record

ReviewSchizophrenia research2015

GABA receptor subunit distribution and FMRP-mGluR5 signaling abnormalities in the cerebellum of subjects with schizophrenia, mood disorders, and autism.

S Hossein Fatemi, Timothy D Folsom

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Schizophrenia research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 87 citations in OpenAlex.

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  16. Social Deficits and Cerebellar Degeneration in Purkinje CellFrontiers in molecular neuroscience · 2022
    Article
  17. Review
  18. Genes · 2021
    Review
  19. Article
  20. Review
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 1 institution in 1 country.

S Hossein FatemiDepartment of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St SE, MMC 392, Minneapolis, MN 55455, USA; Department of Neuroscience, University of Minnesota Medical School, 321 Church St. SE, Minneapolis, MN 55455, USA. Electronic address: fatem002@umn.edu.
Timothy D FolsomDepartment of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St SE, MMC 392, Minneapolis, MN 55455, USA. Electronic address: folso013@umn.edu.
University of Minnesota Medical Center · US

Funding

GABAergic and Reelin Deficits in SchizophreniaR01MH086000 · NIMH · UNIVERSITY OF MINNESOTA · PI FATEMI, SEYYED HOSSEIN · 2010 to 2014
$1.7M
GABAergic Dysfunction in AutismR01HD052074 · NICHD · UNIVERSITY OF MINNESOTA · PI FATEMI, SEYYED HOSSEIN · 2007 to 2011
$1.5M
NICHD NIH HHS 3R01HD052074-03S1NICHD NIH HHS 5R01HD052074-01A2NICHD NIH HHS R01 HD052074NIMH NIH HHS 1R01MH086000-01A2NIMH NIH HHS R01 MH086000
6 · The paper itself

Abstract

Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain. GABAergic receptor abnormalities have been documented in several major psychiatric disorders including schizophrenia, mood disorders, and autism. Abnormal expression of mRNA and protein for multiple GABA receptors has also been observed in multiple brain regions leading to alterations in the balance between excitatory/inhibitory signaling in the brain with potential profound consequences for normal cognition and maintenance of mood and perception. Altered expression of GABAA receptor subunits has been documented in fragile X mental retardation 1 (FMR1) knockout mice, suggesting that loss of its protein product, fragile X mental retardation protein (FMRP), impacts GABAA subunit expression. Recent postmortem studies from our laboratory have shown reduced expression of FMRP in the brains of subjects with schizophrenia, bipolar disorder, major depression, and autism. FMRP acts as a translational repressor and, under normal conditions, inhibits metabotropic glutamate receptor 5 (mGluR5)-mediated signaling. In fragile X syndrome (FXS), the absence of FMRP is hypothesized to lead to unregulated mGluR5 signaling, ultimately resulting in the behavioral and intellectual impairments associated with this disorder. Our laboratory has identified changes in mGluR5 expression in autism, schizophrenia, and mood disorders. In the current review article, we discuss our postmortem data on GABA receptors, FMRP, and mGluR5 levels and compare our results with other laboratories. Finally, we discuss the interactions between these molecules and the potential for new therapeutic interventions that target these interconnected signaling systems.

Indexed as

AnimalsAutistic DisorderCerebellumDisease Models, AnimalFragile X Messenger Ribonucleoprotein 1HumansMiceMood DisordersReceptor, Metabotropic Glutamate 5Receptors, GABASchizophreniaSignal TransductionFragile X Messenger Ribonucleoprotein 1Receptor, Metabotropic Glutamate 5Receptors, GABABipolar disorderCerebellumFMRPGABAmGluR5Schizophrenia

Identifiers

PMID25432637
PMCPMC5301472
OpenAlexW2043010186

What OpenQuestion holds

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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.