Evidence map›Paper›PMID 20488644›Full record

ArticleAlcohol (Fayetteville, N.Y.)2010

Repeated third trimester-equivalent ethanol exposure inhibits long-term potentiation in the hippocampal CA1 region of neonatal rats.

Michael P Puglia, C Fernando Valenzuela

Abstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

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  15. Alcohol and the Developing Brain: Why Neurons Die and How Survivors Change.International journal of molecular sciences · 2018
    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 1 institution in 1 country.

Michael P PugliaDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, 87131, USA.
C Fernando Valenzuela
University of New Mexico · US

Funding

Statistical and Data Management Center-Pediatric,Adolescent, and Maternal CTGUM1AI068616 · NIAID · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Sean Scott Brummel, Marlene Ann Cooper · 2011 to 2026
$155.6M
Alcohol and Developing Neuronal CircuitsR01AA015614 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2005 to 2026
$3.9M
Alcohol Research Training in NeurosciencesT32AA014127 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Jonathan L Brigman · 2003 to 2026
$3.3M
Ethanol, Synaptic Transmission, Plasticity in the Developing HippocampusF30AA017813 · NIAAA · UNIVERSITY OF NEW MEXICO · PI PUGLIA, MICHAEL · 2008 to 2011
$133k
NIAAA NIH HHS F30 AA017813NIAAA NIH HHS F30-AA017813NIAAA NIH HHS R01 AA015614NIAAA NIH HHS R01-AA15614NIAAA NIH HHS T32 AA014127NIAAA NIH HHS T32-AA14127NIAID NIH HHS UM1 AI068616
6 · The paper itself

Abstract

Developmental ethanol exposure damages the hippocampus, causing long-lasting learning and memory deficits. Synaptic plasticity mechanisms (e.g., long-term potentiation [LTP]) contribute to synapse formation and refinement during development. We recently showed that acute ethanol exposure inhibits glutamatergic synaptic transmission and N-methyl-d-aspartate receptor (NMDAR)-dependent LTP in the CA1 hippocampal region of postnatal day (P)7-9 rats. The objective of this study was to further characterize the effect of ethanol on LTP in the developing CA1 hippocampus during the third trimester equivalent. To more closely model human ethanol exposure during this period, rat pups were exposed to ethanol vapor (2 or 4.5 g/dL in air, serum ethanol concentrations=96.6-147.2 or 322-395.6 mg/dL) from P2-9 (4h/d). Brain slices were prepared immediately after the end of the 4-h exposure on P7-9 and extracellular electrophysiological recordings were performed 1-7h later under ethanol-free conditions to model early withdrawal. LTP was not different than group-matched controls in the 96.6-147.2mg/dL group; however, it was impaired in the 322-395.6 mg/dL group. Neither alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor (AMPAR)/NMDAR function nor glutamate release were affected in the 322-395.6 mg/dL ethanol exposure group. These data suggest that repeated in vivo exposure to elevated ethanol doses during the third trimester-equivalent period impairs synaptic plasticity, which may alter maturation of hippocampal circuits and ultimately contribute to the long-lasting cognitive deficits associated with fetal alcohol spectrum disorders.

Indexed as

AnimalsAnimals, NewbornCA1 Region, HippocampalCentral Nervous System DepressantsEthanolFemaleLong-Term PotentiationMaleModels, AnimalPregnancyRatsCentral Nervous System DepressantsEthanol

Identifiers

PMID20488644
PMCPMC2916030
OpenAlexW2154619412

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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.