Evidence map›Paper›PMID 20949055›Full record

ArticlePloS one2010

Loss of LMO4 in the retina leads to reduction of GABAergic amacrine cells and functional deficits.

Philippe M Duquette, Xun Zhou, Nida Lerma Yap, Erik J MacLaren, Jesse J Lu, Valerie A Wallace, Hsiao-Huei Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  10. LMO4 is essential for paraventricular hypothalamic neuronal activity and calcium channel expression to prevent hyperphagia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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  14. LIM domain only 4 (LMO4) regulates calcium-induced calcium release and synaptic plasticity in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

7 authors at 3 institutions in 1 country.

Philippe M DuquetteCentre for Stroke Recovery, Neuroscience, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Xun Zhou
Nida Lerma Yap
Erik J MacLaren
Jesse J Lu
Valerie A Wallace
Hsiao-Huei Chen
Ottawa Hospital Research InstituteOttawa Hospital · CAUniversity of Ottawa · CA

Funding

Canadian Institutes of Health Research MOP-179197Canadian Institutes of Health Research RMF92100
6 · The paper itself

Abstract

backgroundLMO4 is a transcription cofactor expressed during retinal development and in amacrine neurons at birth. A previous study in zebrafish reported that morpholino RNA ablation of one of two related genes, LMO4b, increases the size of eyes in embryos. However, the significance of LMO4 in mammalian eye development and function remained unknown since LMO4 null mice die prior to birth. METHODOLOGY/PRINCIPAL

findingsWe observed the presence of a smaller eye and/or coloboma in ∼40% LMO4 null mouse embryos. To investigate the postnatal role of LMO4 in retinal development and function, LMO4 was conditionally ablated in retinal progenitor cells using the Pax6 alpha-enhancer Cre/LMO4flox mice. We found that these mice have fewer Bhlhb5-positive GABAergic amacrine and OFF-cone bipolar cells. The deficit appears to affect the postnatal wave of Bhlhb5+ neurons, suggesting a temporal requirement for LMO4 in retinal neuron development. In contrast, cholinergic and dopaminergic amacrine, rod bipolar and photoreceptor cell numbers were not affected. The selective reduction in these interneurons was accompanied by a functional deficit revealed by electroretinography, with reduced amplitude of b-waves, indicating deficits in the inner nuclear layer of the retina. CONCLUSIONS/SIGNIFICANCE: Inhibitory GABAergic interneurons play a critical function in controlling retinal image processing, and are important for neural networks in the central nervous system. Our finding of an essential postnatal function of LMO4 in the differentiation of Bhlhb5-expressing inhibitory interneurons in the retina may be a general mechanism whereby LMO4 controls the production of inhibitory interneurons in the nervous system.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBase SequenceDNA PrimersEnhancer Elements, Geneticgamma-Aminobutyric AcidHomeodomain ProteinsImmunohistochemistryIn Situ HybridizationLIM Domain ProteinsMiceMice, Inbred C57BLPromoter Regions, GeneticRetinaTranscription FactorsAdaptor Proteins, Signal TransducingDNA Primersgamma-Aminobutyric AcidHomeodomain ProteinsLIM Domain ProteinsLmo4 protein, mouseTranscription Factors

Identifiers

PMID20949055
PMCPMC2951357
OpenAlexW2046858514

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.