Evidence map›Paper›PMID 19673741›Full record

ArticleAlcoholism, clinical and experimental research2009

Ethanol inhibits muscarinic receptor-induced axonal growth in rat hippocampal neurons.

Kathryn L VanDemark, Marina Guizzetti, Gennaro Giordano, Lucio G Costa

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2009. 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
3.8field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  4. Role of Thioredoxin 1 in Impaired Renal Sodium Excretion of hDJournal of the American Heart Association · 2019
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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

4 authors at 1 institution in 2 countries.

Kathryn L VanDemarkDepartment of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA.
Marina Guizzetti
Gennaro Giordano
Lucio G Costa
University of Washington · US

Funding

XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI ALI SHOJAIE · 1995 to 2026
$42.5M
Environmetal Pathology/Toxicology Training ProgramT32ES007032 · NIEHS · UNIVERSITY OF WASHINGTON · PI FAUSTMAN, ELAINE M, ROSENFELD, MICHAEL E · 1985 to 2023
$10.7M
ETHANOL AND PHOSPHOINOSITIDES DURING BRAIN DEVELOPMENTR01AA008154 · NIAAA · UNIVERSITY OF WASHINGTON · PI COSTA, LUCIO G · 1991 to 2011
$3.1M
NIAAA NIH HHS AA08154NIAAA NIH HHS R01 AA008154NIEHS NIH HHS ES07032NIEHS NIH HHS ES07033NIEHS NIH HHS P30 ES007033NIEHS NIH HHS T32 ES007032
6 · The paper itself

Abstract

backgroundIn utero alcohol exposure can lead to fetal alcohol spectrum (FAS) disorders characterized by cognitive and behavioral deficits. In vivo and in vitro studies have shown that ethanol alters neuronal development. One mechanism through which ethanol has been shown to exert its effects is the perturbation of activated signaling cascades. The cholinergic agonist carbachol has been shown to induce axonal outgrowth through intracellular calcium mobilization, protein kinase C (PKC) activation, and ERK1/2 phosphorylation. This study investigated the effect of ethanol on the differentiation of rat hippocampal pyramidal neurons induced by carbachol as a possible mechanism involved in the developmental neurotoxicity of ethanol.

methodsPrenatal rat hippocampal pyramidal neurons were treated with ethanol (50 to 75 mM) in the presence or absence of carbachol for 24 hours. Neurite outgrowth was assessed spectrophotometrically; axonal length was measured in neurons fixed and immunolabeled with the neuron-specific betaIII tubulin antibody; cytotoxicity was analyzed using the thiazolyl blue tetrazolium bromide assay. The effect of ethanol on carbachol-stimulated intracellular calcium mobilization was assessed utilizing the fluorescent calcium probe, Fluo-3AM. The PepTag(R) assay for nonradioactive detection of PKC from Promega was used to measure PKC activity, and ERK1/2 activation was determined by densitometric analysis of Western blots probed for phospo-ERK1/2.

resultsEthanol treatment (50 to 75 mM) caused an inhibition of carbachol-induced axonal growth, without affecting neuronal viability. Neuron treatment for 15 minutes with ethanol did not inhibit the carbachol-stimulated rise in intracellular calcium, while inhibiting PKC activity at the highest tested concentration and ERK1/2 phosphorylation at both the concentrations used in this study. On the other hand, neuron treatment for 24 hours with ethanol significantly inhibited carbachol-induced increase in intracellular calcium.

conclusionsEthanol inhibited carbachol-induced neurite outgrowth by inhibiting PKC and ERK1/2 activation. These effects may be, in part, responsible for some of the cognitive deficits associated with in utero alcohol exposure.

Indexed as

AnimalsAstrocytesAxonsBlotting, WesternCalciumCarbacholCells, CulturedCentral Nervous System DepressantsColoring AgentsCulture Media, ConditionedEthanolFemaleHippocampusImmunohistochemistryMuscarinic AgonistsNeuritesCalciumCarbacholCentral Nervous System DepressantsColoring AgentsCulture Media, ConditionedEthanolMuscarinic AgonistsProtein Kinase CReceptors, MuscarinicTetrazolium SaltsThiazolesthiazolyl blue

Identifiers

PMID19673741
PMCPMC2885893
OpenAlexW2128285386

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.