Evidence map›Paper›PMID 8815902›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996

TrkA, but not TrkC, receptors are essential for survival of sympathetic neurons in vivo.

A M Fagan, H Zhang, S Landis, R J Smeyne, I Silos-Santiago, M Barbacid

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 192 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Transcytosis-mediated anterograde transport of TrkA receptors is necessary for sympathetic neuron development and function.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Innervation in organogenesis.Current topics in developmental biology · 2022
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Going Too Far Is the Same as Falling ShortFrontiers in cellular neuroscience · 2019
    Review
  19. Review
  20. Review

10 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

A M FaganDepartment of Molecular Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543, USA.
H Zhang
S Landis
R J Smeyne
I Silos-Santiago
M Barbacid
Bristol-Myers Squibb (United States) · US

Funding

DEVELOPMENTAL REGULATION OF NEUROPEPTIDE EXPRESSIONR01HD025681 · NICHD · CASE WESTERN RESERVE UNIVERSITY · PI ZIGMOND, RICHARD E · 1989 to 1997
–
NICHD NIH HHS HD 25681
6 · The paper itself

Abstract

Neurotrophins and their signaling receptors, the Trk family of protein tyrosine kinases, play a major role in the development of the mammalian nervous system. To determine the precise stages that require Trk receptor signaling during development of the sympathetic system, we have analyzed the superior cervical ganglion (SCG) of embryonic and postnatal mice defective for each of the known Trk receptors. Transcripts encoding TrkC are detected in early sympathetic development, before the coalescence of the SCG. trkA expression appears at E13.5, becoming robust from E15.5 onward. In contrast, trkC expression decreases significantly after E15.5 and remains detectable only in a small subpopulation of cells. No significant trkB expression could be detected in the SCG at any developmental stage. Ablation of TrkA receptors does not affect neurogenesis, expression of neuronal markers, or initial axonal growth. However, these receptors are absolutely necessary for the survival of sympathetic neurons after E15.5 and for proper innervation of their distal targets. In contrast, mice defective for either TrkC or TrkB tyrosine kinase receptors do not display detectable defects in their SCGs. These results illustrate the differential roles of the Trk family of receptors during SCG development and define a critical role for TrkA signaling in the survival, but not differentiation, of SCG neurons. Moreover, these observations raise the possibility that at least some SCG neurons become neurotrophin-dependent before complete target innervation.

Indexed as

AnimalsAnimals, NewbornCell SurvivalEmbryo, MammalianImmunohistochemistryMiceMice, KnockoutMicroscopy, ElectronNeuronsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Nerve Growth FactorReceptor, trkAReceptor, trkCSympathetic Nervous SystemProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Nerve Growth FactorReceptor, trkAReceptor, trkC

Identifiers

PMID8815902
PMCPMC6579181
OpenAlexW1898112969

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.