Evidence map›Paper›PMID 29753864›Full record

ArticleNeuroscience2018

Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure.

Clark W Bird, Devin H Taylor, Natalie J Pinkowski, G Jill Chavez, C Fernando Valenzuela

Abstract read
In one paragraph

Article in Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
8.3field-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

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

  1. Pooled it
  2. Assessment of GABANeuroscience letters · 2026
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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

5 authors at 1 institution in 1 country.

Clark W BirdDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Devin H TaylorDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Natalie J PinkowskiDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
G Jill ChavezDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
C Fernando ValenzuelaDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA. Electronic address: fvalenzuela@salud.unm.edu.
University of New Mexico · US

Funding

Understanding neurophysiological deficits in response inhibition in children with FASDP50AA022534 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2014 to 2026
$21.5M
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 P50 AA022534NIAAA NIH HHS R37 AA015614
6 · The paper itself

Abstract

Developmental exposure to ethanol leads to a constellation of cognitive and behavioral abnormalities known as Fetal Alcohol Spectrum Disorders (FASDs). Many cell types throughout the central nervous system are negatively impacted by gestational alcohol exposure, including inhibitory, GABAergic interneurons. Little evidence exists, however, describing the long-term impact of fetal alcohol exposure on survival of interneurons within the hippocampal formation, which is critical for learning and memory processes that are impaired in individuals with FASDs. Mice expressing Venus yellow fluorescent protein in inhibitory interneurons were exposed to vaporized ethanol during the third trimester equivalent of human gestation (postnatal days 2-9), and the long-term effects on interneuron numbers were measured using unbiased stereology at P90. In adulthood, interneuron populations were reduced in every hippocampal region examined. Moreover, we found that a single exposure to ethanol at P7 caused robust activation of apoptotic neurodegeneration of interneurons in the hilus, granule cell layer, CA1 and CA3 regions of the hippocampus. These studies demonstrate that developmental ethanol exposure has a long-term impact on hippocampal interneuron survivability, and may provide a mechanism partially explaining deficits in hippocampal function and hippocampus-dependent behaviors in those afflicted with FASDs.

Indexed as

AnimalsBacterial ProteinsCentral Nervous System DepressantsEthanolFemaleFetal Alcohol Spectrum DisordersGABAergic NeuronsHippocampusInterneuronsLuminescent ProteinsMaleMiceMice, Inbred C57BLMice, TransgenicPregnancyPrenatal Exposure Delayed EffectsBacterial ProteinsCentral Nervous System DepressantsEthanolLuminescent Proteinsyellow fluorescent protein, Bacteriaalcoholapoptosisdevelopmentfetalhippocampusinterneuron

Identifiers

PMID29753864
PMCPMC5994377
OpenAlexW2804268458

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.