Evidence map›Paper›PMID 27079797›Full record

ArticleScientific reports2016

INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model.

Lorena Benedetti, Anna Ghilardi, Elsa Rottoli, Marcella De Maglie, Laura Prosperi, Carla Perego, Mirko Baruscotti, Annalisa Bucchi, Luca Del Giacco, Maura Francolini

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-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

23 citing papers in PubMed, 43 citations in OpenAlex.

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  10. Zebrafish as a model organism for neurodegenerative disease.Frontiers in molecular neuroscience · 2022
    Review
  11. Article
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  13. Pathogenic Effect ofNeurology · 2021
    Article
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  20. The Novel Small Molecule TRVA242 Stabilizes Neuromuscular Junction Defects in Multiple Animal Models of Amyotrophic Lateral Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    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

10 authors at 3 institutions in 1 country.

Lorena BenedettiDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Neuroscience Institute, National Research Council (CNR), Via Vanvitelli 32, 20139 Milano, Italy.
Anna GhilardiDepartment of BioSciences, University of Milan, Via Celoria 26, 20133 Milano, Italy.
Elsa RottoliDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Neuroscience Institute, National Research Council (CNR), Via Vanvitelli 32, 20139 Milano, Italy.
Marcella De MaglieDepartment of Veterinary Science and Public Health, University of Milan, Via Celoria 10, 20133 Milano, Italy.
Laura ProsperiDepartment of BioSciences, University of Milan, Via Celoria 26, 20133 Milano, Italy.
Carla PeregoDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Via Trentacoste 2, 20133 Milano, Italy.
Mirko BaruscottiDepartment of BioSciences, University of Milan, Via Celoria 26, 20133 Milano, Italy.
Annalisa BucchiDepartment of BioSciences, University of Milan, Via Celoria 26, 20133 Milano, Italy.
Luca Del GiaccoDepartment of BioSciences, University of Milan, Via Celoria 26, 20133 Milano, Italy.
Maura FrancoliniDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Neuroscience Institute, National Research Council (CNR), Via Vanvitelli 32, 20139 Milano, Italy.
University of Milan · ITNational Research Council · ITNeuroscience Institute · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenic role of SOD1 mutations in amyotrophic lateral sclerosis (ALS) was investigated using a zebrafish disease model stably expressing the ALS-linked G93R mutation. In addition to the main pathological features of ALS shown by adult fish, we found remarkably precocious alterations in the development of motor nerve circuitry and embryo behavior, and suggest that these alterations are prompted by interneuron and motor neuron hyperexcitability triggered by anomalies in the persistent pacemaker sodium current INaP. The riluzole-induced modulation of INaP reduced spinal neuron excitability, reverted the behavioral phenotypes and improved the deficits in motor nerve circuitry development, thus shedding new light on the use of riluzole in the management of ALS. Our findings provide a valid phenotype-based tool for unbiased in vivo drug screening that can be used to develop new therapies.

Indexed as

Action PotentialsAmyotrophic Lateral SclerosisAnimalsAnimals, Genetically ModifiedDisease Models, AnimalGene ExpressionLocomotionMotor ActivityMotor NeuronsMusclesMutationNeuromuscular JunctionPhenotypePhenylglyoxalRiluzoleSpinal CordisonitrosoacetophenonePhenylglyoxalRiluzoleSuperoxide Dismutase

Identifiers

PMID27079797
PMCPMC4832213
OpenAlexW2339404916

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.