Evidence map›Paper›PMID 34095364›Full record

ArticleNeurobiology of stress2021

Early life adversity targets the transcriptional signature of hippocampal NG2+ glia and affects voltage gated sodium (Na

Giulia Treccani, Hatice Yigit, Thomas Lingner, Vanessa Schleuβner, Franziska Mey, Michael A van der Kooij, Malin Wennström, David P Herzog, Matthias Linke, Markus Fricke and 5 more

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of stress, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

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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

15 authors at 4 institutions in 3 countries.

Giulia TreccaniDepartment of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Hatice YigitCellular Neurobiology, Institute for Developmental Biology and Neurobiology, Johannes Gutenberg-University of Mainz, Mainz, Germany.
Thomas LingnerGenevention GmbH, Göttingen, Germany.
Vanessa SchleuβnerCellular Neurobiology, Institute for Developmental Biology and Neurobiology, Johannes Gutenberg-University of Mainz, Mainz, Germany.
Franziska MeyDepartment of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Michael A van der KooijDepartment of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Malin WennströmDepartment of Clinical Sciences Malmö, Clinical Memory Research Unit, The Wallenberg Lab, Lund University, Malmö, Sweden.
David P HerzogDepartment of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Matthias LinkeInstitute for Human Genetics, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Markus FrickeGenevention GmbH, Göttingen, Germany.
Michael J SchmeisserInstitute for Microscopic Anatomy and Neurobiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Gregers WegenerTranslational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Thomas MittmannInstitute of Physiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Jacqueline TrotterCellular Neurobiology, Institute for Developmental Biology and Neurobiology, Johannes Gutenberg-University of Mainz, Mainz, Germany.
Marianne B MüllerDepartment of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Johannes Gutenberg University Mainz · DEGenevention (Germany) · DEAarhus University · DKLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The precise mechanisms underlying the detrimental effects of early life adversity (ELA) on adult mental health remain still elusive. To date, most studies have exclusively targeted neuronal populations and not considered neuron-glia crosstalk as a crucially important element for the integrity of stress-related brain function. Here, we have investigated the impact of ELA, in the form of a limited bedding and nesting material (LBN) paradigm, on a glial subpopulation with unique properties in brain homeostasis, the NG2+ cells. First, we have established a link between maternal behavior, activation of the offspring's stress response and heterogeneity in the outcome to LBN manipulation. We further showed that LBN targets the hippocampal NG2+ transcriptome with glucocorticoids being an important mediator of the LBN-induced molecular changes. LBN altered the NG2+ transcriptome and these transcriptional effects were correlated with glucocorticoids levels. The functional relevance of one LBN-induced candidate gene,

Indexed as

Early life stressNav-channelsNG2+ gliaScn7aTranscriptomeTranslational psychiatry

Identifiers

PMID34095364
PMCPMC8164094
OpenAlexW3162043068

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.