Evidence map›Paper›PMID 10377349›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Functionally antagonistic interactions between the TrkA and p75 neurotrophin receptors regulate sympathetic neuron growth and target innervation.

J Kohn, R S Aloyz, J G Toma, M Haak-Frendscho, F D Miller

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 174 citations in OpenAlex.

  1. Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022
    Review
  2. Review
  3. Article
  4. Article
  5. p75NTR and DR6 Regulate Distinct Phases of Axon Degeneration Demarcated by Spheroid Rupture.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Villainous role of estrogen in macrophage-nerve interaction in endometriosis.Reproductive biology and endocrinology : RB&E · 2018
    Review
  11. Implication of the neurotrophin receptor p75Expert review of ophthalmology · 2017
    Article
  12. Review
  13. Molecular Mechanisms of Sympathetic Remodeling and Arrhythmias.Circulation. Arrhythmia and electrophysiology · 2016
    Review
  14. Review
  15. Article
  16. Coronin-1 and calcium signaling governs sympathetic final target innervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  17. Review
  18. Review
  19. Review
  20. 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

5 authors at 3 institutions in 2 countries.

J KohnCentre for Neuronal Survival, Montréal Neurological Institute, McGill University, Montréal, Québec, Canada, H3A 2B4.
R S Aloyz
J G Toma
M Haak-Frendscho
F D Miller
Montreal Neurological Institute and Hospital · CAMcGill University · CAPromega (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this report, we provide evidence that NGF and BDNF have functionally antagonistic actions on sympathetic neuron growth and target innervation, with NGF acting via TrkA to promote growth and BDNF via p75NTR to inhibit growth. Specifically, in cultured sympathetic neurons that themselves synthesize BDNF, exogenous BDNF inhibits and function-blocking BDNF antibodies enhance process outgrowth. Both exogenous and autocrine BDNF mediate this effect via p75NTR because (1) BDNF does not inhibit growth of neurons lacking p75NTR, (2) function-blocking p75NTR antibodies enhance NGF-mediated growth, and (3) p75NTR-/- sympathetic neurons grow more robustly in response to NGF than do their wild-type counterparts. To determine the physiological relevance of this functional antagonism, we examined the pineal gland, a well defined sympathetic target organ. BDNF is present in the pineal gland during target innervation, and incoming sympathetic axons are p75NTR positive. Moreover, the pineal glands of BDNF+/- and BDNF-/- mice are hyperinnervated with sympathetic fibers, and tyrosine hydroxylase (TH) levels are elevated. Increased tyrosine hydroxylase is also observed in the BDNF+/- carotid artery, another sympathetic neuron target. Thus, BDNF, made by sympathetic neurons and/or their target organs, acts via p75NTR to antagonize NGF-mediated growth and target innervation, suggesting that sympathetic target innervation is determined by the balance of positively and negatively acting neurotrophins present in developing and potentially mature targets.

Indexed as

AnimalsAntibodiesAutocrine CommunicationAxonsBrain-Derived Neurotrophic FactorCarotid ArteriesCell DivisionCells, CulturedCell SurvivalGene DeletionGenotypeMiceMice, KnockoutNerve Growth FactorsNeuritesNeuronsAntibodiesBrain-Derived Neurotrophic FactorNerve Growth FactorsReceptor, Nerve Growth FactorReceptors, Nerve Growth FactorReceptor, trkATyrosine 3-Monooxygenase

Identifiers

PMID10377349
PMCPMC6782315
OpenAlexW1855182844

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.