Evidence map›Paper›PMID 27242215›Full record

ArticleAlcoholism, clinical and experimental research2016

Chronic Gestational Exposure to Ethanol Leads to Enduring Aberrances in Cortical Form and Function in the Medial Prefrontal Cortex.

Alexander G J Skorput, Hermes H Yeh

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
9.8field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Prefrontal Interneurons: Populations, Pathways, and Plasticity Supporting Typical and Disordered Cognition in Rodent Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  13. Article
  14. Article
  15. Development of prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
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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

2 authors at 2 institutions in 1 country.

Alexander G J SkorputDepartment of Neuroscience, University of Minnesota Medical School Twin Cities, Minneapolis, Minnesota.
Hermes H YehDepartment of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire.
Dartmouth–Hitchcock Medical Center · USUniversity of Minnesota · US

Funding

Ethanol Exposure In Utero and Interneuronopathy in the Medial Prefrontal CortexR01AA023410 · NIAAA · DARTMOUTH COLLEGE · PI YEH, HERMES H · 2014 to 2018
$1.9M
Pharmacologically targeting the NKCC1 chloride cotransporter in utero for FASDR21AA024036 · NIAAA · DARTMOUTH COLLEGE · PI YEH, HERMES H · 2015 to 2016
$425k
NIAAA NIH HHS R01 AA023410NIAAA NIH HHS R21 AA024036
6 · The paper itself

Abstract

backgroundExposure to ethanol (EtOH) in utero alters the disposition of tangentially migrating GABAergic interneurons in the fetal brain. The medial ganglionic eminence (MGE) gives rise to a large portion of cortical GABAergic interneurons, including the parvalbumin-expressing interneurons that shape and contribute to inhibitory/excitatory (I/E) balance of the intracortical circuit. Here, we investigated in the mouse medial prefrontal cortex (mPFC) the hypothesis that low levels of maternal EtOH consumption from closure of the neural tube embryonic day (E) 9.5 until birth result in an enduring interneuronopathy.

methodsPregnant mice were subjected to a 2% w/w EtOH consumption regimen starting at neural tube closure and ending at parturition. Neurogenesis in the MGE was assessed by 5-bromo-2-deoxyuridine (BrdU) immunofluorescence at E12.5. The count and distribution of parvalbumin-expressing interneurons were determined in adult animals, and patch clamp electrophysiology was performed to determine GABAergic function and I/E balance. Open-field behavior in adult mice was assessed to determine whether the EtOH-exposed cohort displayed a lasting alteration in exploratory behavior.

resultsIn embryos exposed to EtOH in utero, we found increased BrdU labeling in the MGE, pointing to increased neurogenesis. Adult mice prenatally exposed to EtOH were hyperactive, and this was associated with an increase in parvalbumin-expressing GABAergic interneurons in the mPFC. In addition, prenatal EtOH exposure altered the balance between spontaneous inhibitory and excitatory synaptic input and attenuated GABAergic tone in layer V mPFC pyramidal neurons in juvenile mice.

conclusionsThese findings underscore that altered migration of GABAergic interneurons contributes to the EtOH-induced aberration of cortical development and that these effects persist into adulthood as altered cortical form and function.

Indexed as

Alcohol DrinkingAnimalsCell MovementEthanolExploratory BehaviorFemaleGABAergic NeuronsInterneuronsMaleMiceMice, TransgenicNeurogenesisPrefrontal CortexPregnancyPrenatal Exposure Delayed EffectsEthanolCortical DevelopmentFetal Alcohol Spectrum DisordersGABAInhibitory/Excitatory BalanceMedial Prefrontal Cortex

Identifiers

PMID27242215
PMCPMC5559699
OpenAlexW2415149133

What OpenQuestion holds

Textmetadata
LicenceTDM
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.