Evidence map›Paper›PMID 27281270›Full record

ArticleInvestigative ophthalmology & visual science2016

Vulnerability of Dopaminergic Amacrine Cells to Chronic Ischemia in a Mouse Model of Oxygen-Induced Retinopathy.

Nathan J Spix, Lei-Lei Liu, Zhijing Zhang, Joshua P Hohlbein, Cameron L Prigge, Shravan Chintala, Christophe P Ribelayga, Dao-Qi Zhang

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2016. 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
2.0field-weighted citation impact, top 14% 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, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Nathan J SpixEye Research Institute Oakland University, Rochester, Michigan, United States.
Lei-Lei LiuEye Research Institute Oakland University, Rochester, Michigan, United States.
Zhijing ZhangRuiz Department of Ophthalmology and Visual Science, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States.
Joshua P HohlbeinEye Research Institute Oakland University, Rochester, Michigan, United States.
Cameron L PriggeEye Research Institute Oakland University, Rochester, Michigan, United States.
Shravan ChintalaEye Research Institute Oakland University, Rochester, Michigan, United States.
Christophe P RibelaygaRuiz Department of Ophthalmology and Visual Science, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States 3Graduate School of Biomedical Sciences, The University of Texas Health Science Center at.
Dao-Qi ZhangEye Research Institute Oakland University, Rochester, Michigan, United States.
Oakland University · USSmith-Kettlewell Eye Research Institute · USThe University of Texas Health Science Center at Houston · US

Funding

VISION RESEARCHP30EY010608 · NEI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MASSEY, STEPHEN C · 1994 to 2014
$7.9M
Circadian Clock Function in the Mammalian RetinaR01EY018640 · NEI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI RIBELAYGA, CHRISTOPHE P. · 2009 to 2015
$2.0M
Functional organization of the retinal dopaminergic networkR01EY022640 · NEI · OAKLAND UNIVERSITY · PI ZHANG, DAO-QI · 2014 to 2018
$1.8M
NEI NIH HHS P30 EY010608NEI NIH HHS R01 EY018640NEI NIH HHS R01 EY022640
6 · The paper itself

Abstract

purposeRetinal dopamine deficiency is a potential cause of myopia and visual deficits in retinopathy of prematurity (ROP). We investigated the cellular mechanisms responsible for lowered levels of retinal dopamine in an oxygen-induced retinopathy (OIR) mouse model of ROP.

methodsRetinopathy was induced by exposing mice to 75% oxygen from postnatal day 7 (P7) to P12. Oxygen-induced retinopathy and age-matched control mice were euthanized at P12, P17, P25, or P42 to P50. Immunohistochemistry, electrophysiology, and biochemical approaches were used to determine the effect of OIR on the structure and function of dopaminergic amacrine cells (DACs).

resultsThe total number of DACs was unchanged in OIR retinas at P12 despite significant capillary dropout in the central retina. However, a significant loss of DACs was observed in P17 OIR retinas (in which neovascularization was maximal), with the cell loss being more profound in the central (avascular) than in the peripheral (neovascular) regions. Cell loss was persistent in both regions at P25, at which time retinal neovascularization had regressed. At P42, the percentage of DACs lost (54%) was comparable to the percent decrease in total dopamine content (53%). Additionally, it was found that DACs recorded in OIR retinas at P42 to P50 had a complete dendritic field and exhibited relatively normal spontaneous and light-induced electrical activity.

conclusionsThe results suggest that remaining DACs are structurally and functionally intact and that loss of DACs is primarily responsible for the decreased levels of retinal dopamine observed after OIR.

Indexed as

Amacrine CellsAnalysis of VarianceAnimalsAnimals, NewbornBlotting, WesternDisease Models, AnimalDopamineImmunohistochemistryIschemiaMiceMice, Inbred C57BLOxygenRetinaRetinal NeovascularizationRetinal VesselsRetinopathy of PrematurityDopamineOxygen

Identifiers

PMID27281270
PMCPMC4913805
OpenAlexW2412714736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.