Evidence map›Paper›PMID 21335065›Full record

ArticleNeuroscience2011

L1 cell adhesion molecule promotes resistance to alcohol-induced silencing of growth cone responses to guidance cues.

B Sepulveda, I Carcea, B Zhao, S R J Salton, D L Benson

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Understanding variability in ethanol teratogenicity.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

5 authors at 1 institution in 1 country.

B SepulvedaFishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
I Carcea
B Zhao
S R J Salton
D L Benson
Icahn School of Medicine at Mount Sinai · US

Funding

Training Program in NeuroscienceT32MH087004 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GEORGE W. HUNTLEY · 2009 to 2026
$4.0M
L1 function and sensitivity to ethanolR01AA014898 · NIAAA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BENSON, DEANNA L · 2005 to 2009
$1.9M
Mechanisms of Axon Outgrowth and TargetingR01NS050634 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BENSON, DEANNA L · 2007 to 2010
$1.5M
Advanced Microscopy Shared Resource FacilityR24CA095823 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDRICH, VICTOR LOUIS · 2002 to 2006
$1.3M
CONFOCAL MICROSCOPE FACILITYS10RR009145 · NCRR · MOUNT SINAI SCHOOL OF MEDICINE OF CUNY · PI MASUR, SANDRA K · 1994 to 1994
–
NCI NIH HHS 5R24 CA095823-04NCI NIH HHS R24 CA095823NCRR NIH HHS 1 S10 RR0 9145-01NIAAA NIH HHS R01 AA014898NIAAA NIH HHS R01AA01497NIMH NIH HHS 5T32MH087004NIMH NIH HHS T32 MH087004NINDS NIH HHS NS050634NINDS NIH HHS R01 NS050634
6 · The paper itself

Abstract

Alcohol exposure in utero is a common cause of mental retardation, but the targets and mechanisms of action are poorly understood. Several lines of data point toward alterations in cortical connectivity, suggesting that axon guidance may be vulnerable to alcohol exposure. To test this, we asked whether ethanol directly affects cortical axonal growth cone responses to guidance cues. We find that even low concentrations of ethanol (12.5 mM; 57.2 mg/dl) commonly observed in social drinking prevent growth cone responses to three mechanistically independent guidance cues, Semaphorin3A, Lysophosphatidic Acid, and Netrin-1. However, this effect is highly dependent on substrate; axonal growth cones extending on an L1 cell adhesion molecule (L1CAM) substrate retain responsiveness to cues following exposure to ethanol, while those growing on poly-L-lysine or N-cadherin do not. The effects of ethanol on axon extension are, by contrast, quite modest. Quantitative assessments of the effects of ethanol on the surface distribution of L1CAM in growth cones suggest that L1CAM homophilic interactions may be particularly relevant for retaining growth cone responsiveness following ethanol exposure. Together, our findings indicate that ethanol can directly and generally alter growth cone responses to guidance cues, that a substrate of L1CAM effectively antagonizes this effect, and that cortical axonal growth cone vulnerability to ethanol may be predicted in part based on the environment through which they are extending.

Indexed as

AnimalsCells, CulturedCentral Nervous System DepressantsCuesEthanolGrowth ConesImmunohistochemistryLysophospholipidsNerve Growth FactorsNetrin-1Neural Cell Adhesion Molecule L1RatsSemaphorin-3ATumor Suppressor ProteinsCentral Nervous System DepressantsEthanollysophosphatidic acidLysophospholipidsNerve Growth FactorsNetrin-1Neural Cell Adhesion Molecule L1Ntn1 protein, ratSemaphorin-3ATumor Suppressor Proteins

Identifiers

PMID21335065
PMCPMC3070798
OpenAlexW1998311675

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.