Evidence map›Paper›PMID 29907879›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2018

Profiling changes in cortical astroglial cells following chronic stress.

Stephanie Simard, Gianfilippo Coppola, Christopher A Rudyk, Shawn Hayley, Robyn J McQuaid, Natalina Salmaso

Open access · hybridAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 57 citations in OpenAlex.

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  18. Alterations in Astrocytic Regulation of Excitation and Inhibition by Stress Exposure and in Severe Psychopathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
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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

6 authors at 3 institutions in 2 countries.

Stephanie SimardDepartment of Neuroscience, Carleton University, Ottawa, ON, Canada.
Gianfilippo CoppolaChild Study Center, Yale University, New Haven, CT, USA.
Christopher A RudykDepartment of Neuroscience, Carleton University, Ottawa, ON, Canada.
Shawn HayleyDepartment of Neuroscience, Carleton University, Ottawa, ON, Canada.
Robyn J McQuaidThe Royal Ottawa Hospital, Ottawa, ON, Canada.
Natalina SalmasoDepartment of Neuroscience, Carleton University, Ottawa, ON, Canada. natalina.salmaso@carleton.ca.
Carleton University · CAYale University · USRoyal Ottawa Mental Health Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have suggested that cortical astroglia play an important role in depressive-like behaviors. Potential astroglial contributions have been proposed based on their known neuroplastic functions, such as glutamate recycling and synaptic plasticity. However, the specific mechanisms by which astroglial cells may contribute or protect against a depressive phenotype remain unknown. To delineate astroglial changes that accompany depressive-like behavior, we used astroglial-specific bacTRAP mice exposed to chronic variable stress (CVS) and profiled the astroglial translatome using translating ribosome affinity purification (TRAP) in conjunction with RNAseq. As expected, CVS significantly increased anxiety- and depressive-like behaviors and corticosterone levels and decreased GFAP expression in astroglia, although this did not reflect a change in the total number of astroglial cells. TRAPseq results showed that CVS decreased genes associated with astroglial plasticity: RhoGTPases, growth factor signaling, and transcription regulation, and increased genes associated with the formation of extracellular matrices such as perineuronal nets (PNNs). PNNs inhibit neuroplasticity and astroglia contribute to the formation, organization, and maintenance of PNNs. To validate our TRAPseq findings, we showed an increase in PNNs following CVS. Degradation of PNNs in the prefrontal cortex of mice exposed to CVS reversed the CVS-induced behavioral phenotype in the forced swim test. These data lend further support to the neuroplasticity hypothesis of depressive behaviors and, in particular, extend this hypothesis beyond neuronal plasticity to include an overall decrease in genes associated with cortical astroglial plasticity following CVS. Further studies will be needed to assess the antidepressant potential of directly targeting astroglial cell function in models of depression.

Indexed as

Protein BiosynthesisAnimalsAnxietyAstrocytesChronic DiseaseCorticosteroneDepressionGene ExpressionGlial Fibrillary Acidic ProteinMaleMice, Inbred C57BLMice, TransgenicNeuronal PlasticityPrefrontal CortexStress, PsychologicalUncertaintyCorticosteroneGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouse

Identifiers

PMID29907879
PMCPMC6046043
OpenAlexW2805957248

What OpenQuestion holds

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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.