Evidence map›Paper›PMID 22703993›Full record

ArticleAlcohol (Fayetteville, N.Y.)2012

Effects of third trimester-equivalent ethanol exposure on Cl(-) co-transporter expression, network activity, and GABAergic transmission in the CA3 hippocampal region of neonatal rats.

Julie C Everett, Yamhilette Licón-Muñoz, C Fernando Valenzuela

Abstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Fetal alcohol spectrum disorders and neuroimmune changes.International review of neurobiology · 2014
    Review
  14. Moderate prenatal alcohol exposure reduces plasticity and alters NMDA receptor subunit composition in the dentate gyrus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  15. Article
  16. Article
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.

Julie C EverettDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Yamhilette Licón-Muñoz
C Fernando Valenzuela
University of New Mexico · US

Funding

Alcohol and Developing Neuronal CircuitsR01AA015614 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2005 to 2026
$3.9M
Alcohol and Developing Neuronal CircuitsR37AA015614 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI VALENZUELA, CARLOS FERNANDO · 2012 to 2021
$3.5M
NIAAA NIH HHS R01 AA015614NIAAA NIH HHS R01-AA15614NIAAA NIH HHS R37 AA015614
6 · The paper itself

Abstract

Fetal alcohol spectrum disorders are often associated with structural and functional hippocampal abnormalities, leading to long-lasting learning and memory deficits. The mechanisms underlying these abnormalities are not fully understood. Here, we investigated whether ethanol exposure during the 3rd trimester-equivalent period alters spontaneous network activity that is involved in neuronal circuit development in the CA3 hippocampal region. This activity is driven by GABA(A) receptors, which can have excitatory actions in developing neurons as a consequence of greater expression of the Cl(-) importer, NKCC1, with respect to expression of the Cl(-) exporter, KCC2, resulting in high [Cl(-)](i). Rat pups were exposed to ethanol vapor from postnatal day (P) 2-16 (4 h/day). Weight gain was significantly reduced in pups exposed to ethanol compared to control at P15 and 16. Brain slices were prepared immediately after the end of the 4-h exposure on P4-16 and experiments were also performed under ethanol-free conditions at the end of the exposure paradigm (P17-22). Ethanol exposure did not significantly affect expression of KCC2 or NKCC1, nor did it affect network activity in the CA3 hippocampal region. Ethanol exposure significantly decreased the frequency (at P9-11) and increased the amplitude (at P5-8 and P17-21) of GABA(A) receptor-mediated miniature postsynaptic currents. These data suggest that repeated in vivo exposure to ethanol during the 3rd trimester-equivalent period alters GABAergic transmission in the CA3 hippocampal region, an effect that could lead to abnormal circuit maturation and perhaps contribute to the pathophysiology of fetal alcohol spectrum disorders.

Indexed as

AnimalsCA3 Region, HippocampalEthanolFemaleK Cl- CotransportersPregnancyRatsRats, Sprague-DawleyReceptors, GABA-ASodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2SymportersSynaptic TransmissionEthanolK Cl- CotransportersReceptors, GABA-ASlc12a2 protein, ratSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2Symporters

Identifiers

PMID22703993
PMCPMC3411872
OpenAlexW2020206702

What OpenQuestion holds

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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.