Evidence map›Paper›PMID 21839828›Full record

ArticleNeurotoxicology and teratology

Decreased axonal density and altered expression profiles of axonal guidance genes underlying lead (Pb) neurodevelopmental toxicity at early embryonic stages in the zebrafish.

Jun Zhang, Samuel M Peterson, Gregory J Weber, Xinqiang Zhu, Wei Zheng, Jennifer L Freeman

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Retinal toxicity of heavy metals and its involvement in retinal pathology.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Developmental exposure to PbChemosphere · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Developmental lead exposure causes startle response deficits in zebrafish.Aquatic toxicology (Amsterdam, Netherlands) · 2011
    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

6 authors at 2 institutions in 2 countries.

Jun ZhangSchool of Health Sciences, Purdue University, 550 Stadium Mall Drive, West Lafayette, IN 47907, USA.
Samuel M Peterson
Gregory J Weber
Xinqiang Zhu
Wei Zheng
Jennifer L Freeman
Purdue University West Lafayette · USZhejiang University · CN

Funding

Beta-Amyloid Clearance by Mammalian Choroid Plexus: Effect of Lead ExposureR21ES017055 · NIEHS · PURDUE UNIVERSITY · PI ZHENG, WEI · 2009 to 2010
$457k
NIEHS NIH HHS ES017055NIEHS NIH HHS R21 ES017055
6 · The paper itself

Abstract

Previous studies have reported that environmental lead (Pb) exposure can result in neurological alterations in children leading to reduced IQ, attention deficit hyperactivity disorder, and diminished reading and learning abilities. However, the specific alterations in neurodevelopmental morphology and the underlying genetic mechanisms of these alterations have not yet been thoroughly defined. To investigate alterations in neurologic morphology and test the hypothesis that developmental Pb neurotoxicity is partially mediated through alterations in neuronal growth and transport function of axons, the changes of specific axon tracts in the embryonic zebrafish brain were observed with anti-acetylated α-tubulin staining at several developmental time points through 36hours post fertilization (hpf). In addition, the role of a subset of axonogenesis-related genes including shha, epha4b, netrin1b, netrin2, and noiwas investigated with real-time quantitative PCR (qPCR). Pb treatment resulted in decreased axonal density at 18, 20, and 24hpf for specific axon tracts in the midbrain and forebrain. These observations corresponded to an observed down-regulation of shha and epha4b at 14 and 16hpf, respectively. The axonal density in Pb exposed individuals at later stages (30 and 36hpf) was not significantly different from controls. An overexpression of netrin2 at these two developmental stages suggests a novel role for this gene in regulating axonal density specific to Pb neurotoxicity. Although no significant differences in axonal density was observed in the two later developmental stages, further studies are needed to determine if the morphologic alterations observed at the earlier stages will have lasting functional impacts.

Indexed as

AnimalsAxonal TransportAxonsBrainDisease Models, AnimalEmbryo, NonmammalianGene Expression ProfilingGene Expression Regulation, DevelopmentalLead Poisoning, Nervous SystemReal-Time Polymerase Chain ReactionZebrafishZebrafish ProteinsZebrafish Proteins

Identifiers

PMID21839828
PMCPMC3225594
OpenAlexW2016730760

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.