Evidence map›Paper›PMID 29950598›Full record

ArticleCell death & disease2018

Nogo-A inactivation improves visual plasticity and recovery after retinal injury.

Julius Baya Mdzomba, Noémie Jordi, Léa Rodriguez, Sandrine Joly, Frédéric Bretzner, Vincent Pernet

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. 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
0.8field-weighted citation impact, top 34% 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. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Transneuronal Degeneration in the Brain During Glaucoma.Frontiers in aging neuroscience · 2021
    Review
  10. Review
  11. Article
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 2 institutions in 2 countries.

Julius Baya MdzombaCUO-Recherche, Centre de recherche du CHU de Québec and Département d'ophtalmologie, Faculté de médecine, Université Laval, Quebec, QC, Canada.
Noémie JordiDepartment of Health Sciences and Technology, Brain Research Institute, University of Zurich, ETH Zurich, 8057, Zurich, Switzerland.
Léa RodriguezCUO-Recherche, Centre de recherche du CHU de Québec and Département d'ophtalmologie, Faculté de médecine, Université Laval, Quebec, QC, Canada.
Sandrine JolyCUO-Recherche, Centre de recherche du CHU de Québec and Département d'ophtalmologie, Faculté de médecine, Université Laval, Quebec, QC, Canada.
Frédéric BretznerCentre de recherche du CHU de Québec and Département de psychiatrie et neurosciences, Faculté de médecine, Université Laval, Quebec, QC, Canada.
Vincent PernetCUO-Recherche, Centre de recherche du CHU de Québec and Département d'ophtalmologie, Faculté de médecine, Université Laval, Quebec, QC, Canada. vincent.pernet.1@ulaval.ca.ORCID 0000-0002-9618-972X
Université Laval · CAUniversity of Zurich · CH

Funding

Canada Foundation for Innovation (Fondation canadienne pour l'innovation) 34204Fonds de Recherche du Québec - Santé (Fonds de la recherche en sante du Quebec) 30633
6 · The paper itself

Abstract

Myelin-associated proteins such as Nogo-A are major inhibitors of neuronal plasticity that contribute to permanent neurological impairments in the injured CNS. In the present study, we investigated the influence of Nogo-A on visual recovery after retinal injuries in mice. Different doses of N-methyl-D-aspartate (NMDA) were injected in the vitreous of the left eye to induce retinal neuron death. The visual function was monitored using the optokinetic response (OKR) as a behavior test, and electroretinogram (ERG) and local field potential (LFP) recordings allowed to assess changes in retinal and cortical neuron activity, respectively. Longitudinal OKR follow-ups revealed reversible visual deficits after injection of NMDA ≤ 1 nmole in the left eye and concomitant functional improvement in the contralateral visual pathway of the right eye that was let intact. Irreversible OKR loss observed with NMDA ≥ 2 nmol was correlated with massive retinal cell death and important ERG response decline. Strikingly, the OKR mediated by injured and intact eye stimulation was markedly improved in Nogo-A KO mice compared with WT animals, suggesting that the inactivation of Nogo-A promotes visual recovery and plasticity. Moreover, OKR improvement was associated with shorter latency of the N2 wave of Nogo-A KO LFPs relative to WT animals. Strikingly, intravitreal injection of anti-Nogo-A antibody (11C7) in the injured eye exerted positive effects on cortical LFPs. This study presents the intrinsic ability of the visual system to recover from NMDA-induced retinal injury and its limitations. Nogo-A neutralization may promote visual recovery in retinal diseases such as glaucoma.

Indexed as

Neuronal PlasticityRecovery of FunctionAnimalsAntibodies, NeutralizingDown-RegulationElectroretinographyGene Expression RegulationIntravitreal InjectionsMaleMice, Inbred C57BLMice, KnockoutNeurogliaN-MethylaspartateNogo ProteinsRetinaRetinal NeuronsAntibodies, NeutralizingN-MethylaspartateNogo Proteins

Identifiers

PMID29950598
PMCPMC6021388
OpenAlexW2811277922

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.