Evidence map›Paper›PMID 25662716›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

Nogo Receptor 1 Limits Ocular Dominance Plasticity but not Turnover of Axonal Boutons in a Model of Amblyopia.

Michael G Frantz, Ryan J Kast, Hilary M Dorton, Katherine S Chapman, Aaron W McGee

Abstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
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  15. Multiple Roles for Nogo Receptor 1 in Visual System Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016
    Review
  16. Nogo Receptor 1 Confines a Disinhibitory Microcircuit to the Critical Period in Visual Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
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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

5 authors.

Michael G FrantzDevelopmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.
Ryan J KastDevelopmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.
Hilary M DortonDevelopmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.
Katherine S ChapmanDevelopmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.
Aaron W McGeeDevelopmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.

Funding

Deciphering Inhibition of Visual Plasticity by NgR1R01EY021580 · NEI · UNIVERSITY OF LOUISVILLE · PI MCGEE, AARON W · 2012 to 2020
$3.1M
NEI NIH HHS 1R01EY021580NEI NIH HHS R01 EY021580
6 · The paper itself

Abstract

The formation and stability of dendritic spines on excitatory cortical neurons are correlated with adult visual plasticity, yet how the formation, loss, and stability of postsynaptic spines register with that of presynaptic axonal varicosities is unknown. Monocular deprivation has been demonstrated to increase the rate of formation of dendritic spines in visual cortex. However, we find that monocular deprivation does not alter the dynamics of intracortical axonal boutons in visual cortex of either adult wild-type (WT) mice or adult NgR1 mutant (ngr1-/-) mice that retain critical period visual plasticity. Restoring normal vision for a week following long-term monocular deprivation (LTMD), a model of amblyopia, partially restores ocular dominance (OD) in WT and ngr1-/- mice but does not alter the formation or stability of axonal boutons. Both WT and ngr1-/- mice displayed a rapid return of normal OD within 8 days after LTMD as measured with optical imaging of intrinsic signals. In contrast, single-unit recordings revealed that ngr1-/- exhibited greater recovery of OD by 8 days post-LTMD. Our findings support a model of structural plasticity in which changes in synaptic connectivity are largely postsynaptic. In contrast, axonal boutons appear to be stable during changes in cortical circuit function.

Indexed as

Dominance, OcularNeuronal PlasticityAmblyopiaAnimalsDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsNogo Receptor 1Presynaptic TerminalsSensory DeprivationVisual AcuityVisual CortexNogo Receptor 1axonboutonelectrophysiologyin vivo imaginglong-term monocular deprivationoptical imaging

Identifiers

PMID25662716
PMCPMC4830283

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.