Evidence map›Paper›PMID 25313866›Full record

ArticleeLife2014

Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis.

Félix Leroy, Boris Lamotte d'Incamps, Rebecca D Imhoff-Manuel, Daniel Zytnicki

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 162 citations in OpenAlex.

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  6. bioRxiv : the preprint server for biology · 2026
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  7. Review
  8. Review
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  10. Machine-Learning Classification of Motor Unit Types in the Adult Mouse.bioRxiv : the preprint server for biology · 2025
    Article
  11. Review
  12. Article
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  16. Review
  17. Review
  18. Postnatal survival of phrenic motor neurons is promoted by BDNF/TrkB.FL signaling.Journal of applied physiology (Bethesda, Md. : 1985) · 2024
    Article
  19. Article
  20. Article

44 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Félix LeroyLaboratory of Neurophysics and Physiology, UMR 8119, Paris Descartes University, Paris, France.
Boris Lamotte d'IncampsLaboratory of Neurophysics and Physiology, UMR 8119, Paris Descartes University, Paris, France.ORCID http://orcid.org/0000-0003-4221-7526
Rebecca D Imhoff-ManuelLaboratory of Neurophysics and Physiology, UMR 8119, Paris Descartes University, Paris, France.
Daniel ZytnickiLaboratory of Neurophysics and Physiology, UMR 8119, Paris Descartes University, Paris, France.
Université Paris Cité · FR

Funding

Electrical and mechanical properties of motor units in a mouse model of ALSR01NS077863 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HECKMAN, CHARLES · 2011 to 2015
$2.6M
NINDS NIH HHS R01 NS077863NINDS NIH HHS R01NS077863
6 · The paper itself

Abstract

In amyotrophic lateral sclerosis (ALS) the large motoneurons that innervate the fast-contracting muscle fibers (F-type motoneurons) are vulnerable and degenerate in adulthood. In contrast, the small motoneurons that innervate the slow-contracting fibers (S-type motoneurons) are resistant and do not degenerate. Intrinsic hyperexcitability of F-type motoneurons during early postnatal development has long been hypothesized to contribute to neural degeneration in the adult. Here, we performed a critical test of this hypothesis by recording from identified F- and S-type motoneurons in the superoxide dismutase-1 mutant G93A (mSOD1), a mouse model of ALS at a neonatal age when early pathophysiological changes are observed. Contrary to the standard hypothesis, excitability of F-type motoneurons was unchanged in the mutant mice. Surprisingly, the S-type motoneurons of mSDO1 mice did display intrinsic hyperexcitability (lower rheobase, hyperpolarized spiking threshold). As S-type motoneurons are resistant in ALS, we conclude that early intrinsic hyperexcitability does not contribute to motoneuron degeneration.

Indexed as

Action PotentialsAmyotrophic Lateral SclerosisAnimalsBiomarkersDendritesDisease Models, AnimalDNA-Binding ProteinsMatrix Metalloproteinase 9Mice, TransgenicMotor NeuronsMutationNerve DegenerationNerve Tissue ProteinsNuclear ProteinsReceptors, EstrogenRNA, MessengerBiomarkersDNA-Binding Proteinsestrogen receptor-related receptor betaMatrix Metalloproteinase 9Nerve Tissue ProteinsNeuN protein, mouseNuclear ProteinsReceptors, EstrogenRNA, MessengerSlc17a7 protein, mouseSuperoxide DismutaseVesicular Glutamate Transport Protein 1ALShyperexcitabilitymotoneuronmouseneuroscience

Identifiers

PMID25313866
PMCPMC4227046
OpenAlexW2133232170

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.