Evidence map›Paper›PMID 10662836›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Stabilization of growing retinal axons by the combined signaling of nitric oxide and brain-derived neurotrophic factor.

A F Ernst, G Gallo, P C Letourneau, S C McLoon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 108 citations in OpenAlex.

  1. Intrinsic organization of the corpus callosum.Frontiers in physiology · 2024
    Review
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  13. Nitric oxide synthase regulates morphogenesis of zebrafish spinal cord motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
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  19. Signaling from blood vessels to CNS axons through nitric oxide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  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

4 authors at 1 institution in 1 country.

A F ErnstDepartment of Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455, USA.
G Gallo
P C Letourneau
S C McLoon
University of Minnesota · US

Funding

MECHANISMS OF NERVE GROWTH CONE TURNING AND BRANCHINGR01HD019950 · NICHD · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LETOURNEAU, PAUL C. · 1985 to 2013
$3.2M
DEVELOPMENT OF PATTERNED VISUAL CONNECTIONS IN THE BRAINR01EY011926 · NEI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MCLOON, STEVEN C · 1997 to 1999
–
NEI NIH HHS EY11926NICHD NIH HHS HD19950NICHD NIH HHS R01 HD019950
6 · The paper itself

Abstract

The pattern of axonal projections early in the development of the nervous system lacks the precision present in the adult. During a developmental process of refinement, mistargeted projections are eliminated while correct projections are retained. Previous studies suggest that during development nitric oxide (NO) is involved in the elimination of mistargeted retinal axons, whereas brain-derived neurotrophic factor (BDNF) may stabilize retinal axon arbors. It is unclear whether these neuromodulators interact. This study showed that NO induced growth cone collapse and retraction of developing retinal axons. This effect was not attributable to NO-induced neurotoxicity. BDNF protected growth cones and axons from the effects of NO. This effect was specific to BDNF, because neither nerve growth factor (NGF) nor neurotrophin-3 (NT-3) prevented NO-induced growth cone collapse and axon retraction. Exposure to both BDNF and NO, but not either factor alone, stabilized growth cones and axons. Stabilized axons exhibited minimal retraction or extension. This response appears to be a new axon "state" and not simply a partial amelioration of the effect of NO, because lower doses of BDNF or NO allowed axon extension. Furthermore, BDNF/NO-induced growth cone stabilization correlated with the appearance of a cytochalasin D-resistant population of actin filaments. BDNF protection from NO likely was mediated locally at the level of the growth cone, because growth cones or individual filopodia in contact with BDNF-coated beads were protected from NO-induced collapse. These findings suggest a cellular mechanism by which some axonal connections are stabilized and some are eliminated during development.

Indexed as

AnimalsAxonsBrain-Derived Neurotrophic FactorCells, CulturedChick EmbryoGanglia, SpinalHeartHydrazinesMolsidomineNeuronsNeurotrophin 3Nitric OxideNitric Oxide DonorsOrgan Culture TechniquesRetinaSignal Transduction3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamineBrain-Derived Neurotrophic FactorHydrazineslinsidomineMolsidomineNeurotrophin 3Nitric OxideNitric Oxide Donors

Identifiers

PMID10662836
PMCPMC6772364
OpenAlexW1647008873

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.