Evidence map›Paper›PMID 17549747›Full record

ArticleJournal of neuroscience research2007

No effect of genetic deletion of contactin-associated protein (CASPR) on axonal orientation and synaptic plasticity.

Anilkumar M Pillai, German P Garcia-Fresco, Aurea D Sousa, Jeffrey L Dupree, Benjamin D Philpot, Manzoor A Bhat

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Paranodal Axoglial Junctions, an Essential Component in Axonal Homeostasis.Frontiers in cell and developmental biology · 2022
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. In vivo deletion of immunoglobulin domains 5 and 6 in neurofascin (Nfasc) reveals domain-specific requirements in myelinated axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  7. Review
  8. Article
  9. Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  10. Myelination and regional domain differentiation of the axon.Results and problems in cell differentiation · 2009
    Review
  11. 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.

Anilkumar M PillaiDepartment of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA.
German P Garcia-Fresco
Aurea D Sousa
Jeffrey L Dupree
Benjamin D Philpot
Manzoor A Bhat
University of North Carolina at Chapel Hill · USNeuroDevelopment Center · USVirginia Commonwealth University · US

Funding

Molecular Organization &Function of Paranodal JunctionsR01GM063074 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BHAT, MANZOOR A. · 2001 to 2023
$5.8M
VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
Molecular Characterization of Axon-Glial InteractionsR01NS050356 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BHAT, MANZOOR A. · 2006 to 2016
$2.9M
NIGMS NIH HHS GM63074NIGMS NIH HHS R01 GM063074NINDS NIH HHS 5P30NS047463NINDS NIH HHS P30 NS047463NINDS NIH HHS R01 NS050356
6 · The paper itself

Abstract

Myelinated axons are endowed with a specialized domain structure that is essential for saltatory action potential conduction. The paranodal domain contains the axoglial junctions and displays a unique ultrastructure that resembles the invertebrate septate junctions (SJs). Biochemical characterizations of the paranodal axoglial SJs have identified several molecular components that include Caspr and contactin (Cont) on the axonal side and neurofascin 155 kDa (NF155) isoform on the glial side. All these proteins are essential for the formation of the axoglial SJs. Based on the interactions between Caspr and Cont and their colocalization in the CA1 synaptic areas, it was proposed that the synaptic function of Cont requires Caspr. Here we have extended the phenotypic analysis of CASPR mutants to address further the role of Caspr at the axoglial SJs and also in axonal orientation and synaptic plasticity. We report that, in CASPR mutants, the smooth endoplasmic reticulum (SER) forms elongated membranous complexes that accumulate at the nodal/paranodal region and stretch into the juxtaparanodal region, a defect that is consistent with the paranodal disorganization. We show that the cerebellar microorganization is unaffected in CASPR mutants. We also demonstrate that Caspr function is not essential for normal CA1 synaptic transmission and plasticity. Taken together with previous findings, our results highlight that the Caspr/Cont complex is essential for the formation of axoglial SJs, whereas Cont may regulate axonal orientation and synaptic plasticity independent of its association with Caspr.

Indexed as

AnimalsAxonsCell Adhesion Molecules, NeuronalCerebellumContactinsEndoplasmic Reticulum, SmoothExcitatory Postsynaptic PotentialsFluorescent Antibody TechniqueGene DeletionHippocampusMiceMice, KnockoutMicroscopy, ConfocalMicroscopy, Electron, TransmissionNeuronal PlasticitySynaptic TransmissionCell Adhesion Molecules, NeuronalCntnap1 protein, mouseContactins

Identifiers

PMID17549747
PMCPMC2824167
OpenAlexW2002705524

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.