Evidence map›Paper›PMID 24048844›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Dendrite complexity of sympathetic neurons is controlled during postnatal development by BMP signaling.

Afsaneh Majdazari, Jutta Stubbusch, Christian M Müller, Melanie Hennchen, Marlen Weber, Chu-Xia Deng, Yuji Mishina, Günther Schütz, Thomas Deller, Hermann Rohrer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. A low affinityeLife · 2020
    Article
  8. Article
  9. Article
  10. Coiled-coil structure-dependent interactions between polyQ proteins and Foxo lead to dendrite pathology and behavioral defects.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Lin28B and Let-7 in the Control of Sympathetic Neurogenesis and Neuroblastoma Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  15. Review
  16. 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

10 authors at 6 institutions in 3 countries.

Afsaneh MajdazariReseach Group Developmental Neurobiology, Max-Planck-Institute for Brain Research, Frankfurt/M, Germany, Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, Frankfurt/M, Germany, Genetics of Development and Disease Branch, NIDDK, NIH, Bethesda, Maryland 20892, Department of Biologic and Materials Sciences, University of Michigan, School of Dentistry, Ann Arbor, Michigan 48109-1078, and Department Molecular Biology of the Cell I German Cancer Research Center, D-69120 Heidelberg, Germany.
Jutta Stubbusch
Christian M Müller
Melanie Hennchen
Marlen Weber
Chu-Xia Deng
Yuji Mishina
Günther Schütz
Thomas Deller
Hermann Rohrer
Max Planck Institute for Brain Research · DEMax Planck Society · DEUniversity of Michigan–Ann Arbor · USGoethe University Frankfurt · DEInstitute of Neuroimmunology of the Slovak Academy of Sciences · SKNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendrite development is controlled by the interplay of intrinsic and extrinsic signals affecting initiation, growth, and maintenance of complex dendrites. Bone morphogenetic proteins (BMPs) stimulate dendrite growth in cultures of sympathetic, cortical, and hippocampal neurons but it was unclear whether BMPs control dendrite morphology in vivo. Using a conditional knock-out strategy to eliminate Bmpr1a and Smad4 in immature noradrenergic sympathetic neurons we now show that dendrite length, complexity, and neuron cell body size are reduced in adult mice deficient of Bmpr1a. The combined deletion of Bmpr1a and Bmpr1b causes no further decrease in dendritic features. Sympathetic neurons devoid of Bmpr1a/1b display normal Smad1/5/8 phosphorylation, which suggests that Smad-independent signaling paths are involved in dendritic growth control downstream of BMPR1A/B. Indeed, in the Smad4 conditional knock-out dendrite and cell body size are not affected and dendrite complexity and number are increased. Together, these results demonstrate an in vivo function for BMPs in the generation of mature sympathetic neuron dendrites. BMPR1 signaling controls dendrite complexity postnatally during the major dendritic growth period of sympathetic neurons.

Indexed as

Age FactorsAnalysis of VarianceAnimalsAnimals, NewbornArchaeal ProteinsBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsCells, CulturedDendritesDNA-Directed DNA PolymeraseEmbryo, MammalianFluorescent DyesGanglia, SympatheticGene Expression Regulation, DevelopmentalHomeodomain ProteinsImaging, Three-DimensionalArchaeal ProteinsBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsDbh protein, Sulfolobus solfataricusDNA-Directed DNA PolymeraseFluorescent DyesHomeodomain ProteinsMicrotubule-Associated ProteinsMtap2 protein, mouseNBPhox proteinNerve Tissue ProteinsSmad4 ProteinSmad4 protein, mouseTranscription Factors

Identifiers

PMID24048844
PMCPMC3789870
OpenAlexW2039908544

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.