Evidence map›Paper›PMID 18768700›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Sex-specific programming of offspring emotionality after stress early in pregnancy.

Bridget R Mueller, Tracy L Bale

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 460 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
460citing papers in PubMed, 4 pooled it
66.9field-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

460 citing papers in PubMed, 4 syntheses or guidelines pooled it, 982 citations in OpenAlex.

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  17. Neonatal hyperoxia exposure does not exacerbate hypertension programmed by maternal obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
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400 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.

Bridget R MuellerDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Tracy L Bale
University of Pennsylvania · US

Funding

TRAINING PROGRAM IN BEHAVIORAL/COGNITIVE NEUROSCIENCET32MH017168 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI KABLE, JOSEPH W · 1985 to 2018
$4.2M
NIMH NIH HHS T32 MH-017168NIMH NIH HHS T32 MH017168
6 · The paper itself

Abstract

Prenatal stress is associated with an increased vulnerability to neurodevelopmental disorders, including autism and schizophrenia. To determine the critical time window when fetal antecedents may induce a disease predisposition, we examined behavioral responses in offspring exposed to stress during early, mid, and late gestation. We found that male offspring exposed to stress early in gestation displayed maladaptive behavioral stress responsivity, anhedonia, and an increased sensitivity to selective serotonin reuptake inhibitor treatment. Long-term alterations in central corticotropin-releasing factor (CRF) and glucocorticoid receptor (GR) expression, as well as increased hypothalamic-pituitary-adrenal (HPA) axis responsivity, were present in these mice and likely contributed to an elevated stress sensitivity. Changes in CRF and GR gene methylation correlated with altered gene expression, providing important evidence of epigenetic programming during early prenatal stress. In addition, we found the core mechanism underlying male vulnerability may involve sex-specific placenta responsivity, where stress early in pregnancy significantly increased expression of PPARalpha (peroxisome proliferator-activated receptor alpha), IGFBP-1 (insulin-like growth factor binding protein 1), HIF3alpha (hypoxia-inducible factor 3a), and GLUT4 (glucose transporter 4) in male placentas but not females. Examination of placental epigenetic machinery revealed basal sex differences, providing further evidence that sex-specific programming begins very early in pregnancy, and may contribute to the timing and vulnerability of the developing fetus to maternal perturbations. Overall, these results indicate that stress experience early in pregnancy may contribute to male neurodevelopmental disorders through impacts on placental function and fetal development.

Indexed as

Prenatal Exposure Delayed EffectsSex CharacteristicsAnalysis of VarianceAnimalsAnimals, NewbornBehavior, AnimalCorticotropin-Releasing HormoneEmotionsExploratory BehaviorFemaleFood PreferencesHindlimb SuspensionHypothalamo-Hypophyseal SystemMaleMiceMice, Inbred C57BLCorticotropin-Releasing HormoneReceptor, Serotonin, 5-HT1AReceptors, GlucocorticoidSerotonin Plasma Membrane Transport ProteinsSucroseTph2 protein, mouseTryptophan Hydroxylase

Identifiers

PMID18768700
PMCPMC2731562
OpenAlexW1994740828

What OpenQuestion holds

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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.