Evidence map›Paper›PMID 25600109›Full record

ArticleMolecular psychiatry2015

Somatostatin, neuronal vulnerability and behavioral emotionality.

L C Lin, E Sibille

Open access · greenAbstract read
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. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
6.2field-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

122 citing papers in PubMed, 188 citations in OpenAlex.

  1. Trial
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  7. Molecular Characterization of the Progressive Landscape of Depression.bioRxiv : the preprint server for biology · 2026
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  8. Review
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  13. GABADrug design, development and therapy · 2026
    Review
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62 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 1 institution in 1 country.

L C LinTranslational Neuroscience Program, Department of Psychiatry, Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.
E Sibille1] Translational Neuroscience Program, Department of Psychiatry, Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA [2] Departments of Psychiatry, Pharmacology and Toxicology, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, ON, Canada.
University of Pittsburgh · US

Funding

Transcriptome analysis in major depressionR01MH077159 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MCCLUNG, COLLEEN A, SIBILLE, ETIENNE L · 2007 to 2015
$3.2M
Molecular Aging of the Human Brain: Genetic Modulation and Functional OutcomesR01MH093723 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIBILLE, ETIENNE L · 2011 to 2015
$2.6M
Molecular characterization of a corticolimbic network in depressionK02MH084060 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIBILLE, ETIENNE L · 2009 to 2013
$589k
NIMH NIH HHS K02 MH084060NIMH NIH HHS MH077159NIMH NIH HHS MH084060NIMH NIH HHS MH093723NIMH NIH HHS R01 MH077159NIMH NIH HHS R01 MH093723
6 · The paper itself

Abstract

Somatostatin (SST) deficits are common pathological features in depression and other neurological disorders with mood disturbances, but little is known about the contribution of SST deficits to mood symptoms or causes of these deficits. Here we show that mice lacking SST (Sst(KO)) exhibit elevated behavioral emotionality, high basal plasma corticosterone and reduced gene expression of Bdnf, Cortistatin and Gad67, together recapitulating behavioral, neuroendocrine and molecular features of human depression. Studies in Sst(KO) and heterozygous (Sst(HZ)) mice show that elevated corticosterone is not sufficient to reproduce the behavioral phenotype, suggesting a putative role for Sst cell-specific molecular changes. Using laser capture microdissection, we show that cortical SST-positive interneurons display significantly greater transcriptome deregulations after chronic stress compared with pyramidal neurons. Protein translation through eukaryotic initiation factor 2 (EIF2) signaling, a pathway previously implicated in neurodegenerative diseases, was most affected and suppressed in stress-exposed SST neurons. We then show that activating EIF2 signaling through EIF2 kinase inhibition mitigated stress-induced behavioral emotionality in mice. Taken together, our data suggest that (1) low SST has a causal role in mood-related phenotypes, (2) deregulated EIF2-mediated protein translation may represent a mechanism for vulnerability of SST neurons and (3) that global EIF2 signaling has antidepressant/anxiolytic potential.

Indexed as

AdenineAnimalsAntidepressive AgentsBrain-Derived Neurotrophic FactorCorticosteroneDisease Models, AnimalEukaryotic Initiation Factor-2FemaleGene Expression RegulationGlutamate DecarboxylaseGreen Fluorescent ProteinsGyrus CinguliIndolesMaleMiceMice, Inbred C57BL7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo(2,3-d)pyrimidin-4-amineAdenineAntidepressive AgentsBrain-Derived Neurotrophic FactorCorticosteroneEukaryotic Initiation Factor-2Glutamate Decarboxylaseglutamate decarboxylase 1Green Fluorescent ProteinsIndolesSomatostatin

Identifiers

PMID25600109
PMCPMC4355106
OpenAlexW2053813762

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.