Evidence map›Paper›PMID 9412489›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Amphiphysin I antisense oligonucleotides inhibit neurite outgrowth in cultured hippocampal neurons.

O Mundigl, G C Ochoa, C David, V I Slepnev, A Kabanov, P De Camilli

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.9field-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

32 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Steering neuronal growth cones by shifting the imbalance between exocytosis and endocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  7. Article
  8. Review
  9. Article
  10. Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. The BAR domain proteins: molding membranes in fission, fusion, and phagy.Microbiology and molecular biology reviews : MMBR · 2006
    Review
  17. Article
  18. Impaired synaptic plasticity and learning in mice lacking beta-adducin, an actin-regulating protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  19. Article
  20. Review
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

6 authors at 3 institutions in 1 country.

O MundiglDepartment of Cell Biology and Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, New Haven, Connecticut 06510, USA.
G C Ochoa
C David
V I Slepnev
A Kabanov
P De Camilli
Yale University · USHoward Hughes Medical Institute · USUniversity of Nebraska Medical Center · US

Funding

ROLE OF YPT5 INTERACTING COMPONENTS IN ENDOCYTOSISP01CA046128 · NCI · YALE UNIVERSITY · PI NOVICK, PETER JAY · 1988 to 2007
$9.5M
NCI NIH HHS CA46128
6 · The paper itself

Abstract

Amphiphysin I is an SH3 domain-containing neuronal protein, enriched in axon terminals, which was reported to act as a physiological binding partner for dynamin I in synaptic vesicle endocytosis. Rvs167 and Rvs161, the yeast homologs of amphiphysin I, have been implicated in endocytosis, actin function, and cell polarity. Now we have explored the possibility that amphiphysin I also may have a role in actin dynamics and cell polarity by testing the effect of amphiphysin I suppression on neurite outgrowth. Freshly plated hippocampal neurons were exposed to antisense oligonucleotides via a new delivery system based on a polycationic amphipathic polymer, PS980. Western blot analysis revealed that amphiphysin I levels steadily increased with neuronal differentiation, whereas in antisense-treated cultures amphiphysin I levels were reduced to approximately 10% of control levels at 48 hr. Concomitantly, a collapse of growth cones and a severe inhibition of neurite outgrowth and axon formation were observed. A similar effect was observed previously after dynamin I suppression in the same culture system (). We also have found that amphiphysin I and dynamin I colocalize in developing neurons at all developmental stages and that a pool of both proteins is colocalized with actin patches at the leading edge of growth cones. Our findings suggest a conserved role of the amphiphysin protein family in the dynamics of the cortical cell cytoskeleton and provide new evidence for a close functional link between amphiphysin I and dynamin I.

Indexed as

Calcium-Binding ProteinsActinsAnimalsCells, CulturedDynamin IDynaminsEndocytosisGene ExpressionGTP PhosphohydrolasesHippocampusMembrane GlycoproteinsMiceNerve Tissue ProteinsNeuritesOligonucleotides, AntisensePhosphoric Monoester HydrolasesActinsamphiphysinCalcium-Binding ProteinsDynamin IDynaminsGTP PhosphohydrolasesMembrane GlycoproteinsNerve Tissue ProteinsOligonucleotides, AntisensePhosphoric Monoester HydrolasesRNA, MessengersynaptojaninSynaptotagminsTubulin

Identifiers

PMID9412489
PMCPMC6793426
OpenAlexW2151766851

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.