Evidence map›Paper›PMID 21429942›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Strain-specific vulnerability to alcohol exposure in utero via hippocampal parent-of-origin expression of deiodinase-III.

Laura J Sittig, Pradeep K Shukla, Laura B K Herzing, Eva E Redei

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  4. Maternal background alters the penetrance of growth phenotypes and sex-specific placental adaptation of offspring sired by alcohol-exposed males.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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  16. Prenatal alcohol exposure alters methyl metabolism and programs serotonin transporter and glucocorticoid receptor expression in brain.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
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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

4 authors at 2 institutions in 1 country.

Laura J SittigDepartment of Psychiatry and Behavioral Sciences, The Asher Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Pradeep K Shukla
Laura B K Herzing
Eva E Redei
Asher Consulting (United States) · USNorthwestern University · US

Funding

Prenatal Alcohol;Hormone-Regulated Genes &BehaviorR01AA013452 · NIAAA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI REDEI, EVA E · 2002 to 2010
$2.3M
Epigenetic Consequences of Prenatal Alcohol ExposureR01AA017978 · NIAAA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI REDEI, EVA E · 2009 to 2014
$1.8M
Hormonal Programming and Epigenetic Imprinting in FAEF31AA018251 · NIAAA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SITTIG, LAURA J. · 2009 to 2011
$89k
NIAAA NIH HHS F31 AA018251NIAAA NIH HHS R01 AA013452NIAAA NIH HHS R01 AA017978
6 · The paper itself

Abstract

Prenatal exposure to alcohol is thought to be the most prevalent nongenetic cause of a wide range of neurodevelopmental deficits. Insufficient thyroid hormone levels are one mechanism that hampers development of the alcohol-exposed brain, and we hypothesized that altered dosage of the imprinted thyroid hormone-inactivating gene deiodinase-III (Dio3) is responsible. To follow parent-of-origin allelic expression of Dio3 in the fetal and adult offspring of alcohol-consuming and control dams, we reciprocally crossed 2 polymorphic rat strains. In the frontal cortex, prenatal alcohol exposure altered imprinting patterns and total expression of Dio3 in the fetus and produced a permanent hypothyroid milieu in the adult. In the hippocampus, alcohol affected the paternal and total expression of Dio3 in the fetus and in the adult male, where thyroid hormone levels were concomitantly increased. Hippocampus-dependent behavioral deficits were identified exclusively in males, suggesting they are dependent on aberrant allelic Dio3 expression. None of these effects were observed in offspring of the reciprocal cross. Thus, genetic background and sex modify vulnerability to prenatal alcohol via brain region-specific expression of Dio3. This finding implies that phenotypic heterogeneity in human fetal alcohol spectrum disorder can be linked to genetic vulnerability in affected brain regions.

Indexed as

AnimalsBlotting, WesternCentral Nervous System DepressantsCrosses, GeneticEthanolFemaleFetal Alcohol Spectrum DisordersGene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicHippocampusHumansIodide PeroxidaseMalePregnancyPrenatal Exposure Delayed EffectsRatsCentral Nervous System DepressantsEthanolIodide PeroxidaseTriiodothyronine

Identifiers

PMID21429942
PMCPMC3114527
OpenAlexW2122579597

What OpenQuestion holds

Textmetadata
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.