Evidence map›Paper›PMID 25426021›Full record

ArticleFrontiers in cellular neuroscience2014

BDNF-induced nitric oxide signals in cultured rat hippocampal neurons: time course, mechanism of generation, and effect on neurotrophin secretion.

Richard Kolarow, Christoph R W Kuhlmann, Thomas Munsch, Christoph Zehendner, Tanja Brigadski, Heiko J Luhmann, Volkmar Lessmann

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  6. The physiology of regulated BDNF release.Cell and tissue research · 2020
    Review
  7. Review
  8. Article
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  13. Article
  14. Mechanisms and regulation of neurotrophin synthesis and secretion.Neurosciences (Riyadh, Saudi Arabia) · 2016
    Review
  15. 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 3 institutions in 1 country.

Richard KolarowMedical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
Christoph R W KuhlmannUniversity Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
Thomas MunschMedical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany.
Christoph ZehendnerUniversity Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
Tanja BrigadskiMedical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
Heiko J LuhmannUniversity Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
Volkmar LessmannMedical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DEOtto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BDNF and nitric oxide signaling both contribute to plasticity at glutamatergic synapses. However, the role of combined signaling of both pathways at the same synapse is largely unknown. Using NO imaging with diaminofluoresceine in cultured hippocampal neurons we analyzed the time course of neurotrophin-induced NO signals. Application of exogenous BDNF, NT-4, and NT-3 (but not NGF) induced NO signals in the soma and in proximal dendrites of hippocampal neurons that were sensitive to NO synthase activity, TrkB signaling, and intracellular calcium elevation. The effect of NO signaling on neurotrophin secretion was analyzed in BDNF-GFP, and NT-3-GFP transfected hippocampal neurons. Exogenous application of the NO donor sodium-nitroprusside markedly inhibited neurotrophin secretion. However, endogenously generated NO in response to depolarization and neurotrophin stimulation, both did not result in a negative feedback on neurotrophin secretion. These results suggest that a negative feedback of NO signaling on synaptic secretion of neurotrophins operates only at high intracellular levels of nitric oxide that are under physiological conditions not reached by depolarization or BDNF signaling.

Indexed as

BDNFneurotrophinsnitric oxidepeptide secretionPSD95synaptic plasticityTrkB

Identifiers

PMID25426021
PMCPMC4224130
OpenAlexW2084107579

What OpenQuestion holds

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LicenceCC BY
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.