Evidence map›Paper›PMID 23175819›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

DSCAM contributes to dendrite arborization and spine formation in the developing cerebral cortex.

Kristen R Maynard, Elke Stein

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  8. Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023
    Article
  9. Article
  10. Article
  11. DSCAM Deficiency Leads to Premature Spine Maturation and Autism-like Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Alterations of presynaptic proteins in autism spectrum disorder.Frontiers in molecular neuroscience · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Article
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  19. ZebrafishThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
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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.

Kristen R MaynardDepartment of Molecular, Cellular and Developmental Biology, Cell Biology and Interdisciplinary Neuroscience Program, Yale University, New Haven, Connecticut 06520, USA.
Elke Stein
Yale University · US

Funding

Interdepartmental Neuroscience Program (INP)T32NS041228 · NINDS · YALE UNIVERSITY · PI Charles A Greer, Marina R Picciotto · 2001 to 2026
$12.0M
PREDOCTORAL TRAINING PROGRAM IN DEVELOPMENTAL BIOLOGYT32HD007180 · NICHD · YALE UNIVERSITY · PI IRISH, VIVIAN · 1985 to 2009
$3.4M
NICHD NIH HHS T32 HD007180NINDS NIH HHS T32 NS041228NINDS NIH HHS T32 NS41228
6 · The paper itself

Abstract

Down syndrome cell adhesion molecule, or DSCAM, has been implicated in many neurodevelopmental processes including axon guidance, dendrite arborization, and synapse formation. Here we show that DSCAM plays an important role in regulating the morphogenesis of cortical pyramidal neurons in the mouse. We report that DSCAM expression is developmentally regulated and localizes to synaptic plasma membranes during a time of robust cortical dendrite arborization and spine formation. Analysis of mice that carry a spontaneous mutation in DSCAM (DSCAM(del17)) revealed gross morphological changes in brain size and shape in addition to subtle changes in cortical organization, volume, and lamination. Early postnatal mutant mice displayed a transient decrease in cortical thickness, but these reductions could not be attributed to changes in neuron production or cell death. DSCAM(del17) mutants showed temporary impairments in the branching of layer V pyramidal neuron dendrites at P10 and P17 that recovered to normal by adulthood. Defects in DSCAM(del17) dendrite branching correlated with a temporal increase in apical branch spine density and lasting changes in spine morphology. At P15 and P42, mutant mice displayed a decrease in the percentage of large, stable spines and an increase in the percentage of small, immature spines. Together, our findings suggest that DSCAM contributes to pyramidal neuron morphogenesis by regulating dendrite arborization and spine formation during cortical circuit development.

Indexed as

AnimalsAntimetabolitesBlotting, WesternBromodeoxyuridineCell Adhesion MoleculesCells, CulturedCerebral CortexDendritesDendritic SpinesFemaleFlow CytometryFluorescent Antibody TechniqueGene Expression Regulation, DevelopmentalIn Situ HybridizationIn Situ Nick-End LabelingMaleAntimetabolitesBromodeoxyuridineCell Adhesion MoleculesDscam protein, mouseRNA, Messenger

Identifiers

PMID23175819
PMCPMC6621782
OpenAlexW2040305049

What OpenQuestion holds

Textmetadata
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.