Evidence map›Paper›PMID 26169973›Full record

ArticleMolecular psychiatry2015

Sex differences in glutamate receptor gene expression in major depression and suicide.

A L Gray, T M Hyde, A Deep-Soboslay, J E Kleinman, M S Sodhi

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 115 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 6 pooled it
10.3field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 6 syntheses or guidelines pooled it, 252 citations in OpenAlex.

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  16. Advancing past ketamine: emerging glutamatergic compounds for the treatment of depression.European archives of psychiatry and clinical neuroscience · 2025
    Review
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55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

A L GrayDepartment of Pharmacy Practice and Center for Pharmaceutical Biotechnology, College of Pharmacy, University of Illinois at Chicago, Chicago, IL, USA.
T M HydeLieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA.
A Deep-SoboslayLieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA.
J E KleinmanLieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA.
M S SodhiDepartment of Pharmacy Practice and Center for Pharmaceutical Biotechnology, College of Pharmacy, University of Illinois at Chicago, Chicago, IL, USA.ORCID http://orcid.org/0000-0002-8261-3040
Johns Hopkins University · USUniversity of Illinois Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating data indicate that the glutamate system is disrupted in major depressive disorder (MDD), and recent clinical research suggests that ketamine, an antagonist of the N-methyl-d-aspartate (NMDA) glutamate receptor (GluR), has rapid antidepressant efficacy. Here we report findings from gene expression studies of a large cohort of postmortem subjects, including subjects with MDD and controls. Our data reveal higher expression levels of the majority of glutamatergic genes tested in the dorsolateral prefrontal cortex (DLPFC) in MDD (F21,59=2.32, P=0.006). Posthoc data indicate that these gene expression differences occurred mostly in the female subjects. Higher expression levels of GRIN1, GRIN2A-D, GRIA2-4, GRIK1-2, GRM1, GRM4, GRM5 and GRM7 were detected in the female patients with MDD. In contrast, GRM5 expression was lower in male MDD patients relative to male controls. When MDD suicides were compared with MDD non-suicides, GRIN2B, GRIK3 and GRM2 were expressed at higher levels in the suicides. Higher expression levels were detected for several additional genes, but these were not statistically significant after correction for multiple comparisons. In summary, our analyses indicate a generalized disruption of the regulation of the GluRs in the DLPFC of females with MDD, with more specific GluR alterations in the suicides and in the male groups. These data reveal further evidence that, in addition to the NMDA receptor, the AMPA, kainate and the metabotropic GluRs may be targets for the development of rapidly acting antidepressant drugs.

Indexed as

AdultCase-Control StudiesFemaleGene ExpressionGlutamic AcidHumansKetamineMajor Depressive DisorderMalePrefrontal CortexReceptors, GlutamateReceptors, N-Methyl-D-AspartateSex FactorsSuicideTranscriptomeGlutamic AcidKetamineReceptors, GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID26169973
OpenAlexW892371344

What OpenQuestion holds

Textmetadata
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.