Evidence map›Paper›PMID 16467531›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Loss of leukemia inhibitory factor receptor beta or cardiotrophin-1 causes similar deficits in preganglionic sympathetic neurons and adrenal medulla.

Stephan Oberle, Andreas Schober, Verena Meyer, Bettina Holtmann, Christopher Henderson, Michael Sendtner, Klaus Unsicker

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. New Concepts of Regeneration and Renewal of Adrenal Chromaffin Cells.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Progressive postnatal motoneuron loss in mice lacking GDF-15.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  10. Mechanism of shortened bones in mucopolysaccharidosis VII.Molecular genetics and metabolism · 2009
    Article
  11. Age-dependent regulation of chromaffin cell proliferation by growth factors, dehydroepiandrosterone (DHEA), and DHEA sulfate.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  12. 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

7 authors at 4 institutions in 2 countries.

Stephan OberleNeuroanatomy and Interdisciplinary Center for Neurosciences, University of Heidelberg, D-69120 Heidelberg, Germany.
Andreas Schober
Verena Meyer
Bettina Holtmann
Christopher Henderson
Michael Sendtner
Klaus Unsicker
Heidelberg University · DEUniversity of Würzburg · DECenter for Neurosciences · USColumbia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukemia inhibitory factor (LIF) receptor beta (LIFRbeta) is a receptor for a variety of neurotrophic cytokines, including LIF, ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1). These cytokines play an essential role for the survival and maintenance of developing and postnatal somatic motoneurons. CNTF may also serve the maintenance of autonomic, preganglionic sympathetic neurons (PSNs) in the spinal cord, as suggested by its capacity to prevent their death after destruction of one of their major targets, the adrenal medulla. Although somatic motoneurons and PSNs share a common embryonic origin, they are distinct in several respects, including responses to lesions. We have studied PSNs in mice with targeted deletions of the LIFRbeta or CT-1 genes, respectively. We show that LIF, CNTF, and CT-1 are synthesized in embryonic adrenal gland and spinal cord and that PSNs express LIFRbeta. In embryonic day 18.5 LIFRbeta (-/-) and CT-1 (-/-) mice, PSNs were reduced by approximately 20%. PSNs projecting to the adrenal medulla were more severely affected (-55%). Although LIFRbeta (-/-) mice revealed normal numbers of adrenal chromaffin cells and axons terminating on chromaffin cells, levels of adrenaline and numbers of adrenaline-synthesizing cells were significantly reduced. We conclude that activation of LIFRbeta is required for normal development of PSNs and one of their prominent targets, the adrenal medulla. Thus, both somatic motoneurons and PSNs in the spinal cord depend on LIFRbeta signaling for their development and maintenance, although PSNs seem to be overall less affected than somatic motoneurons by LIFRbeta deprivation.

Indexed as

ActinsAdrenal MedullaAnimalsBenzenesulfonamidesBenzylaminesCytokinesDizocilpine MaleateHippocampusInterleukin-6Leukemia Inhibitory FactorMiceNerve FibersNeuronsOligopeptidesProtein Kinase InhibitorsSulfonamidesActinsarginyl-glycyl-aspartic acidBenzenesulfonamidesBenzylaminescardiotrophin 1CytokinesDizocilpine MaleateInterleukin-6KN 93Leukemia Inhibitory FactorLif protein, mouseOligopeptidesProtein Kinase InhibitorsSulfonamides

Identifiers

PMID16467531
PMCPMC6793615
OpenAlexW2030830282

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.