Evidence map›Paper›PMID 27391320›Full record

ArticleThe Journal of comparative neurology2019

Brn3a and Brn3b knockout mice display unvaried retinal fine structure despite major morphological and numerical alterations of ganglion cells.

Miruna Georgiana Ghinia, Elena Novelli, Szilard Sajgo, Tudor Constantin Badea, Enrica Strettoi

Open access · greenAbstract read
In one paragraph

Article in The Journal of comparative neurology, 2019. 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
1.0field-weighted citation impact, top 21% 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, 15 citations in OpenAlex.

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  11. A Novel Reporter Mouse Uncovers Endogenous Brn3b Expression.International journal of molecular sciences · 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

5 authors at 4 institutions in 3 countries.

Miruna Georgiana GhiniaNeuroscience Institute of the Italian National Research Council, Pisa Research Campus, 56124, Pisa, Italy.
Elena NovelliNeuroscience Institute of the Italian National Research Council, Pisa Research Campus, 56124, Pisa, Italy.
Szilard SajgoRetinal CIrcuit Development & Genetics Unit, Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, 20892.
Tudor Constantin BadeaRetinal CIrcuit Development & Genetics Unit, Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, 20892.
Enrica StrettoiNeuroscience Institute of the Italian National Research Council, Pisa Research Campus, 56124, Pisa, Italy.
National Institutes of Health · USBabeș-Bolyai University · ROIstituto di Scienza e Tecnologie dell'Informazione "Alessandro Faedo" · ITNeuroscience Institute · IT

Funding

Retinal Circuit Development & GeneticsZIAEY000504 · NEI · NATIONAL EYE INSTITUTE · PI BADEA, TUDOR · 2011 to 2021
$15.6M
Intramural NIH HHS ZIA EY000504
6 · The paper itself

Abstract

Ganglion cells (GCs), the retinal output neurons, receive synaptic inputs from bipolar and amacrine cells in the inner plexiform layer (IPL) and send information to the brain nuclei via the optic nerve. Although GCs constitute less than 1% of the total retinal cells, they occur in numerous types and are the first neurons formed during retinal development. Using Brn3a and Brn3b mutant mice in which the alkaline phosphatase gene was knocked-in (Badea et al. [Neuron] 2009;61:852-864; Badea and Nathans [Vision Res] 2011;51:269-279), we studied the general effects after gene removal on the retinal neuropil together with the consequences of lack of development of large numbers of GCs onto the remaining retinal neurons of the same class. We analyzed the morphology, number, and general architecture of various neuronal types presynaptic to GCs, searching for changes secondary to the decrement in the number of their postsynaptic partners, as well as the morphology and distribution of retinal astrocytes, for their strong topographical relation to GCs. We found that, despite GC losses, retinal organization in Brn3 null mice is remarkably similar to that of wild-type controls. J. Comp. Neurol. 527:187-211, 2019. © 2016 Wiley Periodicals, Inc.

Indexed as

AnimalsHomeodomain ProteinsMiceMice, KnockoutRetinaRetinal Ganglion CellsTranscription Factor Brn-3ATranscription Factor Brn-3BHomeodomain ProteinsPou4f1 protein, mousePou4f2 protein, mouseTranscription Factor Brn-3ATranscription Factor Brn-3BAB_10000340AB_10013783AB_2079751AB_2278725AB_2314052AB_2492226AB_2533912AB_390204AB_399431AB_477035AB_477345Brn3 transcription factorsganglion cellsinner plexiform layermosaicsRRIDs: AB_94166synapses

Identifiers

PMID27391320
PMCPMC5219957
OpenAlexW2493596175

What OpenQuestion holds

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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.