Evidence map›Paper›PMID 26005040›Full record

ArticleExperimental eye research2016

Aberrant activity in retinal degeneration impairs central visual processing and relies on Cx36-containing gap junctions.

Elena Ivanova, Christopher W Yee, Robert Baldoni, Botir T Sagdullaev

Abstract read
In one paragraph

Article in Experimental eye research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  7. Bridging the gap of vision restoration.Frontiers in cellular neuroscience · 2024
    Review
  8. Article
  9. Article
  10. Connexins Biology in the Pathophysiology of Retinal Diseases.Advances in experimental medicine and biology · 2023
    Article
  11. Implications of Neural Plasticity in Retinal Prosthesis.Investigative ophthalmology & visual science · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Altered Expression of GJD2 Messenger RNA and the Coded Protein Connexin 36 in Negative Lens-induced Myopia of Guinea Pigs.Optometry and vision science : official publication of the American Academy of Optometry · 2020
    Article
  19. Article
  20. Network Architecture of Gap Junctional Coupling among Parallel Processing Channels in the Mammalian Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    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

4 authors at 2 institutions in 1 country.

Elena IvanovaDepartments of Ophthalmology and Neurology, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA.
Christopher W YeeDepartments of Ophthalmology and Neurology, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA.
Robert BaldoniDepartments of Ophthalmology and Neurology, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA.
Botir T SagdullaevDepartments of Ophthalmology and Neurology, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA. Electronic address: bos2005@med.cornell.edu.
Burke Medical Research Institute · USCornell University · US

Funding

Retinal neural processing during retinal degenerative diseasesR01EY020535 · NEI · WINIFRED MASTERSON BURKE MED RES INST · PI SAGDULLAEV, BOTIR T. · 2010 to 2014
$2.4M
NEI NIH HHS R01 EY020535
6 · The paper itself

Abstract

In retinal degenerative disease (RD), the diminished light signal from dying photoreceptors has been considered the sole cause of visual impairment. Recent studies show a 10-fold increase in spontaneous activity in the RD network, challenging this paradigm. This aberrant activity forms a new barrier for the light signal, and not only exacerbates the loss of vision, but also may stand in the way of visual restoration. This activity originates in AII amacrine cells and relies on excessive activation of gap junctions. However, it remains unclear whether aberrant activity affects central visual processing and what mechanisms lead to this excessive activation of gap junctions. By combining genetic manipulation with electrophysiological recordings of light-induced activity in both living mice and isolated wholemount retina, we demonstrate that aberrant activity extends along retinotectal projections to alter activity in higher brain centers. Next, to selectively eliminate Cx36-containing gap junctions, which are the primary type expressed by AII amacrine cells, we crossed rd10 mice, a slow-degenerating model of RD, with Cx36 knockout mice. We found that retinal aberrant activity was reduced in the rd10/Cx36KO mice compared to rd10 controls, a direct evidence for involvement of Cx36-containing gap junctions in generating aberrant activity in RD. These data provide an essential support for future experiments to determine if selectively targeting these gap junctions could be a valid strategy for reducing aberrant activity and restoring light responses in RD.

Indexed as

MutationVision, OcularAmacrine CellsAnimalsConnexinsDNADNA Mutational AnalysisFemaleGap Junction delta-2 ProteinGap JunctionsGenotypeImmunohistochemistryMaleMiceMice, KnockoutRetinal DegenerationConnexinsDNAGap Junction delta-2 ProteinConnexin36rd10Retinal degenerationRetinal remodelingSuperior colliculus

Identifiers

PMID26005040
PMCPMC4655183
OpenAlexW227032276

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.