Evidence map›Paper›PMID 33344732›Full record

ArticleNeurobiology of stress2020

Maternal antioxidant treatment prevents the adverse effects of prenatal stress on the offspring's brain and behavior.

H Scott, T J Phillips, Y Sze, A Alfieri, M F Rogers, V Volpato, C P Case, P J Brunton

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of stress, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Article
  8. Review
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  10. Article
  11. Article
  12. The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023
    Review
  13. Article
  14. Remodulation Effect ofFoods (Basel, Switzerland) · 2023
    Article
  15. Article
  16. Article
  17. Neurosteroids and early-life programming: An updated perspective.Current opinion in endocrine and metabolic research · 2022
    Article
  18. Article
  19. Review
  20. Article
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

8 authors at 4 institutions in 2 countries.

H ScottSchool of Clinical Sciences, University of Bristol, Learning & Research Building, Southmead Hospital, Bristol, BS10 5NB, UK.
T J PhillipsSchool of Clinical Sciences, University of Bristol, Learning & Research Building, Southmead Hospital, Bristol, BS10 5NB, UK.
Y SzeDivision of Neurobiology, The Roslin Institute, University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, UK.
A AlfieriDivision of Neurobiology, The Roslin Institute, University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, UK.
M F RogersIntelligent Systems Laboratory, University of Bristol, Merchant Venturers Building, Woodland Road, Bristol, BS8 1UB, UK.
V VolpatoUK Dementia Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ, UK.
C P CaseSchool of Clinical Sciences, University of Bristol, Learning & Research Building, Southmead Hospital, Bristol, BS10 5NB, UK.
P J BruntonDivision of Neurobiology, The Roslin Institute, University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, UK.
Roslin Institute · GBSouthmead Hospital · GBUK Dementia Research Institute · GBUniversity of Bristol · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal exposure to stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. The mechanisms through which the effects of maternal stress are transmitted to the fetus are unclear, however the placenta, as the interface between mother and fetus, is likely to play a key role. Using a rat model, we investigated a role for placental oxidative stress in conveying the effects of maternal social stress to the fetus and the potential for treatment using a nanoparticle-bound antioxidant to prevent adverse outcomes in the offspring. Maternal psychosocial stress increased circulating corticosterone in the mother, but not in the fetuses. Maternal stress also induced oxidative stress in the placenta, but not in the fetal brain. Blocking oxidative stress using an antioxidant prevented the prenatal stress-induced anxiety phenotype in the male offspring, and prevented sex-specific neurobiological changes, specifically a reduction in dendrite lengths in the hippocampus, as well as reductions in the number of parvalbumin-positive neurons and GABA receptor subunits in the hippocampus and basolateral amygdala of the male offspring. Importantly, many of these effects were mimicked in neuronal cultures by application of placental-conditioned medium or fetal plasma from stressed pregnancies, indicating molecules released from the placenta may mediate the effects of prenatal stress on the fetal brain. Indeed, both placenta-conditioned medium and fetal plasma contained differentially abundant microRNAs following maternal stress, and their predicted targets were enriched for genes relevant to nervous system development and psychiatric disorders. The results highlight placental oxidative stress as a key mediator in transmitting the maternal social stress effects on the offspring's brain and behavior, and offer a potential intervention to prevent stress-induced fetal programming of affective disorders.

Indexed as

AnxietyBasolateral amygdalaCorticosteroneGABA receptorsHippocampusmicroRNAsOxidative stressPlacentaPrenatal stressSex differences

Identifiers

PMID33344732
PMCPMC7739187
OpenAlexW3108748664

What OpenQuestion holds

Textmetadata
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.