Evidence map›Paper›PMID 10341229›Full record

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

Mice deficient for tenascin-R display alterations of the extracellular matrix and decreased axonal conduction velocities in the CNS.

P Weber, U Bartsch, M N Rasband, R Czaniera, Y Lang, H Bluethmann, R U Margolis, S R Levinson, P Shrager, D Montag and 1 more

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 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 242 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Extracellular Matrix in Neural Plasticity and Regeneration.Cellular and molecular neurobiology · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021
    Review
  15. NFrontiers in cell and developmental biology · 2021
    Article
  16. Review
  17. Loss of TNR causes a nonprogressive neurodevelopmental disorder with spasticity and transient opisthotonus.Genetics in medicine : official journal of the American College of Medical Genetics · 2020
    Article
  18. Article
  19. Article
  20. Tenascin-X-Discovery and Early Research.Frontiers in immunology · 2020
    Review

21 more citing papers are in PubMed but not listed here.

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

11 authors at 6 institutions in 3 countries.

P WeberDepartment of Neurobiology, Swiss Federal Institute of Technology, Hönggerberg, CH 8093 Zürich, Switzerland.
U Bartsch
M N Rasband
R Czaniera
Y Lang
H Bluethmann
R U Margolis
S R Levinson
P Shrager
D Montag
M Schachner
Universität Hamburg · DEÉcole Polytechnique Fédérale de Lausanne · CHRoche (Switzerland) · CHUniversity of Rochester Medical Center · USColumbia University Irving Medical Center · USUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-R (TN-R), an extracellular matrix glycoprotein of the CNS, localizes to nodes of Ranvier and perineuronal nets and interacts in vitro with other extracellular matrix components and recognition molecules of the immunoglobulin superfamily. To characterize the functional roles of TN-R in vivo, we have generated mice deficient for TN-R by homologous recombination using embryonic stem cells. TN-R-deficient mice are viable and fertile. The anatomy of all major brain areas and the formation and structure of myelin appear normal. However, immunostaining for the chondroitin sulfate proteoglycan phosphacan, a high-affinity ligand for TN-R, is weak and diffuse in the mutant when compared with wild-type mice. Compound action potential recordings from optic nerves of mutant mice show a significant decrease in conduction velocity as compared with controls. However, at nodes of Ranvier there is no apparent change in expression and distribution of Na+ channels, which are thought to bind to TN-R via their beta2 subunit. The distribution of carbohydrate epitopes of perineuronal nets recognized by the lectin Wisteria floribunda or antibodies to the HNK-1 carbohydrate on somata and dendrites of cortical and hippocampal interneurons is abnormal. These observations indicate an essential role for TN-R in the formation of perineuronal nets and in normal conduction velocity of optic nerve.

Indexed as

AnimalsAxonsCells, CulturedCentral Nervous SystemExtracellular Matrix ProteinsMiceMice, KnockoutMicroscopy, ElectronMyelin-Associated GlycoproteinNerve NetNerve Tissue ProteinsNeural ConductionOptic NerveRanvier's NodesStem CellsTenascinExtracellular Matrix ProteinsMyelin-Associated GlycoproteinNerve Tissue ProteinsTenascintenascin R

Identifiers

PMID10341229
PMCPMC6782606
OpenAlexW2124266106

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.