Evidence map›Paper›PMID 24285895›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Prenatal ethanol exposure disrupts intraneocortical circuitry, cortical gene expression, and behavior in a mouse model of FASD.

Hani El Shawa, Charles W Abbott, Kelly J Huffman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
7.9field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Review
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Chemical Exposure-Induced Developmental Neurotoxicity in Head-Regenerating Schmidtea mediterranea.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Article
  13. Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice.Frontiers in cell and developmental biology · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Article
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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

3 authors at 1 institution in 1 country.

Hani El ShawaDepartment of Psychology and Interdepartmental Neuroscience Program, University of California, Riverside, Riverside, California 92521.
Charles W Abbott
Kelly J Huffman
University of California, Riverside · US

Funding

Prenatal ethanol exposure & neocortex, functional org. & gene expressionR03AA021545 · NIAAA · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI HUFFMAN, KELLY · 2012 to 2013
$147k
NIAAA NIH HHS 1R03AA021545-01NIAAA NIH HHS R03 AA021545
6 · The paper itself

Abstract

In utero ethanol exposure from a mother's consumption of alcoholic beverages impacts brain and cognitive development, creating a range of deficits in the child (Levitt, 1998; Lebel et al., 2012). Children diagnosed with fetal alcohol spectrum disorders (FASD) are often born with facial dysmorphology and may exhibit cognitive, behavioral, and motor deficits from ethanol-related neurobiological damage in early development. Prenatal ethanol exposure (PrEE) is the number one cause of preventable mental and intellectual dysfunction globally, therefore the neurobiological underpinnings warrant systematic research. We document novel anatomical and gene expression abnormalities in the neocortex of newborn mice exposed to ethanol in utero. This is the first study to demonstrate large-scale changes in intraneocortical connections and disruption of normal patterns of neocortical gene expression in any prenatal ethanol exposure animal model. Neuroanatomical defects and abnormal neocortical RZRβ, Id2, and Cadherin8 expression patterns are observed in PrEE newborns, and abnormal behavior is present in 20-d-old PrEE mice. The vast network of neocortical connections is responsible for high-level sensory and motor processing as well as complex cognitive thought and behavior in humans. Disruptions to this network from PrEE-related changes in gene expression may underlie some of the cognitive-behavioral phenotypes observed in children with FASD.

Indexed as

AnimalsBehavior, AnimalCadherinsCell CountCerebral CortexEthanolFemaleFetal Alcohol Spectrum DisordersGene ExpressionInhibitor of Differentiation Protein 2In Vitro TechniquesMiceMicroscopy, FluorescenceNuclear Receptor Subfamily 1, Group F, Member 2Osmolar ConcentrationPregnancyCadherinsCdh8 protein, mouseEthanolIdb2 protein, mouseInhibitor of Differentiation Protein 2Nuclear Receptor Subfamily 1, Group F, Member 2Rorb protein, mouse

Identifiers

PMID24285895
PMCPMC3841455
OpenAlexW2007023810

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.