Evidence map›Paper›PMID 10051665›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Growth factor-mediated Fyn signaling regulates alpha-amino-3- hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor expression in rodent neocortical neurons.

M Narisawa-Saito, A J Silva, T Yamaguchi, T Hayashi, T Yamamoto, H Nawa

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Glutamatergic neurotransmission in the prefrontal cortex mediates the suppressive effect of intra-prelimbic cortical infusion of BDNF on cocaine-seeking.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2016
    Article
  6. Review
  7. Infralimbic BDNF/TrkB enhancement of GluN2B currents facilitates extinction of a cocaine-conditioned place preference.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  8. Article
  9. Article
  10. Gliomas and seizures.Medical hypotheses · 2012
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Positive AMPA receptor modulation rapidly stimulates BDNF release and increases dendritic mRNA translation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Absence of Fyn and Src causes a reeler-like phenotype.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

M Narisawa-SaitoDepartment of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
A J Silva
T Yamaguchi
T Hayashi
T Yamamoto
H Nawa
Cold Spring Harbor Laboratory · USNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Src-family protein tyrosine kinases (PTKs) transduce signals to regulate neuronal development and synaptic plasticity. However, the nature of their activators and molecular mechanisms underlying these neural processes are unknown. Here, we show that brain-derived neurotrophic factor (BDNF) and platelet-derived growth factor enhance expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptor 1 and 2/3 proteins in rodent neocortical neurons via the Src-family PTK(s). The increase in AMPA receptor levels was blocked in cultured neocortical neurons by addition of a Src-family-selective PTK inhibitor. Accordingly, neocortical cultures from Fyn-knockout mice failed to respond to BDNF whereas those from wild-type mice responded. Moreover, the neocortex of young Fyn mutants exhibited a significant in vivo reduction in these AMPA receptor proteins but not in their mRNA levels. In vitro kinase assay revealed that BDNF can indeed activate the Fyn kinase: It enhanced tyrosine phosphorylation of Fyn as well as that of enolase supplemented exogenously. All of these results suggest that the Src-family kinase Fyn, activated by the growth factors, plays a crucial role in modulating AMPA receptor expression during brain development.

Indexed as

Gene Expression RegulationAnimalsBrain-Derived Neurotrophic FactorCells, CulturedCrosses, GeneticEpidermal Growth FactorFibroblast Growth Factor 2Growth SubstancesMiceMice, Inbred C57BLMice, KnockoutNeocortexNeuronsPlatelet-Derived Growth FactorProtein-Tyrosine KinasesProto-Oncogene ProteinsBrain-Derived Neurotrophic FactorEpidermal Growth FactorFibroblast Growth Factor 2Fyn protein, mouseFyn protein, ratGrowth SubstancesPlatelet-Derived Growth FactorProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-fynReceptors, AMPAReceptors, GlutamateReceptors, N-Methyl-D-AspartateRNA, Messengersrc-Family Kinases

Identifiers

PMID10051665
PMCPMC26807
OpenAlexW1969292775

What OpenQuestion holds

Texttitle and abstract
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.