Evidence map›Paper›PMID 27844059›Full record

ArticleeNeuro

Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry.

Emma L Louth, Warren Bignell, Christine L Taylor, Craig D C Bailey

Abstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Defects of Cortical Microcircuits Following Early Exposure to Alcohol.Advances in experimental medicine and biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Gestational ethanol exposure impairs motor skills in female mice through dysregulated striatal dopamine and acetylcholine function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
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.

Emma L LouthDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph , Guelph, Ontario N1G 2W1, Canada.ORCID 0000-0001-5357-1315
Warren BignellDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph , Guelph, Ontario N1G 2W1, Canada.
Christine L TaylorDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph , Guelph, Ontario N1G 2W1, Canada.ORCID 0000-0002-4398-7429
Craig D C BaileyDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph , Guelph, Ontario N1G 2W1, Canada.ORCID 0000-0002-4320-6872

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic prenatal exposure to ethanol can lead to a spectrum of teratogenic outcomes that are classified in humans as fetal alcohol spectrum disorders (FASD). One of the most prevalent and persistent neurocognitive components of FASD is attention deficits, and it is now thought that these attention deficits differ from traditional attention deficit hyperactivity disorder (ADHD) in their quality and response to medication. However, the neuronal mechanisms underlying attention deficits in FASD are not well understood. We show here that after developmental binge-pattern ethanol exposure, adult mice exhibit impaired performance on the five-choice serial reaction time test for visual attention, with lower accuracy during initial training and a higher rate of omissions under challenging conditions of high attention demand. Whole-cell electrophysiology experiments in these same mice find dysregulated pyramidal neurons in layer VI of the medial prefrontal cortex, which are critical for normal attention performance. Layer VI neurons show decreased intrinsic excitability and increased responses to stimulation of both nicotinic acetylcholine receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors. Moreover, although nicotinic acetylcholine responses correlate with performance on the five-choice task in control mice, these relationships are completely disrupted in mice exposed to ethanol during development. These findings demonstrate a novel outcome of developmental binge-pattern ethanol exposure and suggest that persistent alterations to the function of prefrontal layer VI neurons play an important mechanistic role in attention deficits associated with FASD.

Indexed as

AnimalsAttentionBinge DrinkingCentral Nervous System DepressantsDisease Models, AnimalEthanolFemaleFetal Alcohol Spectrum DisordersMaleMice, Inbred C57BLNeural PathwaysNeuronsPrefrontal CortexPregnancyPrenatal Exposure Delayed EffectsRandom AllocationCentral Nervous System DepressantsEthanolReceptors, AMPAReceptors, Nicotinicattentiondevelopmental ethanol exposureelectrophysiologyfetal alcohol spectrum disordersnicotinic receptorsprefrontal cortex

Identifiers

PMID27844059
PMCPMC5099605

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.