Evidence map›Paper›PMID 21273439›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

NrCAM deletion causes topographic mistargeting of thalamocortical axons to the visual cortex and disrupts visual acuity.

Galina P Demyanenko, Thorfinn T Riday, Tracy S Tran, Jasbir Dalal, Eli P Darnell, Leann H Brennaman, Takeshi Sakurai, Martin Grumet, Benjamin D Philpot, Patricia F Maness

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

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  7. Close Homolog of L1 Regulates Dendritic Spine Density in the Mouse Cerebral Cortex Through Semaphorin 3B.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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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

10 authors at 4 institutions in 1 country.

Galina P DemyanenkoDepartment of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Thorfinn T Riday
Tracy S Tran
Jasbir Dalal
Eli P Darnell
Leann H Brennaman
Takeshi Sakurai
Martin Grumet
Benjamin D Philpot
Patricia F Maness
University of North Carolina at Chapel Hill · USRutgers, The State University of New Jersey · USIcahn School of Medicine at Mount Sinai · USThe University of Texas Southwestern Medical Center · US

Funding

UNC Neuroscience Center Research Cores: MicroscopyP30NS045892 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZYLKA, MARK J. · 2003 to 2022
$11.5M
Mechanisms of Developmental Spine Pruning Regulated by IgCAMs and SemaphorinsR01MH113280 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MANESS, PATRICIA F · 2017 to 2021
$1.9M
Mechanisms of Presynaptic Plasticity in Visual CortexR01EY018323 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PHILPOT, BENJAMIN D · 2007 to 2011
$1.8M
Recognition Molecules in Cortical DevelopmentR01NS049109 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MANESS, PATRICIA F · 2005 to 2008
$1.1M
Autism Speaks AS1847Howard Hughes Medical InstituteNEI NIH HHS R01 EY018323NEI NIH HHS R01EY018323NIMH NIH HHS R01 MH113280NINDS NIH HHS 5P30NS045892NINDS NIH HHS P30 NS045892NINDS NIH HHS R01 NS049109
6 · The paper itself

Abstract

NrCAM is a neural cell adhesion molecule of the L1 family that has been linked to autism spectrum disorders, a disease spectrum in which abnormal thalamocortical connectivity may contribute to visual processing defects. Here we show that NrCAM interaction with neuropilin-2 (Npn-2) is critical for semaphorin 3F (Sema3F)-induced guidance of thalamocortical axon subpopulations at the ventral telencephalon (VTe), an intermediate target for thalamic axon sorting. Genetic deletion of NrCAM or Npn-2 caused contingents of embryonic thalamic axons to misproject caudally in the VTe. The resultant thalamocortical map of NrCAM-null mutants showed striking mistargeting of motor and somatosensory thalamic axon contingents to the primary visual cortex, but retinogeniculate targeting and segregation were normal. NrCAM formed a molecular complex with Npn-2 in brain and neural cells, and was required for Sema3F-induced growth cone collapse in thalamic neuron cultures, consistent with a vital function for NrCAM in Sema3F-induced axon repulsion. NrCAM-null mice displayed reduced responses to visual evoked potentials recorded from layer IV in the binocular zone of primary visual cortex (V1), particularly when evoked from the ipsilateral eye, indicating abnormal visual acuity and ocularity. These results demonstrate that NrCAM is required for normal maturation of cortical visual acuity, and suggest that the aberrant projection of thalamic motor and somatosensory axons to the visual cortex in NrCAM-null mutant mice impairs cortical functions.

Indexed as

Visual AcuityAnimalsAxonsCell Adhesion MoleculesEvoked Potentials, VisualFemaleGrowth ConesMaleMembrane ProteinsMiceMice, KnockoutMotor CortexNerve Tissue ProteinsNeuropilin-2Somatosensory CortexThalamusCell Adhesion MoleculesMembrane ProteinsNerve Tissue ProteinsNeuropilin-2Nrcam protein, mouseSema3f protein, mouse

Identifiers

PMID21273439
PMCPMC3037548
OpenAlexW2099242308

What OpenQuestion holds

Textmetadata
LicenceTDM
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.