ArticleeLife2018
Hypoexcitability precedes denervation in the large fast-contracting motor units in two unrelated mouse models of ALS.
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.
- Meta-analysis of biological variables' impact on spinal motoneuron electrophysiology data.Journal of neurophysiology · 2020Pooled it
- Treating age-related loss of muscle mass and function: Where should we be focusing?The Journal of physiology · 2026Review
- Chronic Diazepam Reveals Excessive Homeostatic Gain in SOD1International journal of molecular sciences · 2026Article
- Chronic diazepam reveals excessive homeostatic gain in SOD1bioRxiv : the preprint server for biology · 2026Article
- Spinal motoneuron excitability is homeostatically regulated through β-adrenergic neuromodulation in wild-type and presymptomatic SOD1 mice.Progress in neurobiology · 2026Article
- Machine-learning classification of motor unit types in the adult mouse.The Journal of physiology · 2026Article
- Changes in the Structure of the Neuromuscular Junction and Muscle Fiber Types Following an Acute Injury Model Induced by Eccentric Contraction.Current issues in molecular biology · 2026Article
- Splicing the narrative: alternative TARDBP splicing and its relation to neurodegeneration in ALS and FTD.The Journal of clinical investigation · 2026Review
- Increase in Ia Afferent Synaptic Excitation of SOD1 G93A Mouse Motoneurons by 2-Week Anodal Trans-Spinal Direct Current Stimulation Does Not Ameliorate the Cellular Burden of the Disease.The European journal of neuroscience · 2025Article
- Extracellular Matrix Remodeling in Motor Neuron Diseases.International journal of molecular sciences · 2025Review
- Machine-Learning Classification of Motor Unit Types in the Adult Mouse.bioRxiv : the preprint server for biology · 2025Article
- Integrated profiling of iPSC-derived motor neurons carrying C9orf72, FUS, TARDBP, or SOD1 mutations.Stem cell reports · 2025Article
- Embryonic motor neuron programming factors reactivate immature gene expression and suppress ALS pathologies in postnatal motor neurons.Nature neuroscience · 2025Article
- Motor unit mechanisms of speed control in mouse locomotion.bioRxiv : the preprint server for biology · 2025Article
- Synaptic imbalance and increased inhibition impair motor function in SMA.Science advances · 2025Article
- Trimetazidine stimulates intracellular CaScientific reports · 2025Article
- A Multi-Scale, High-Fidelity Computational Model of the Mouse Triceps Surae Motor Pool.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2025Article
- Article
- The spinal premotor network driving scratching flexor and extensor alternation.bioRxiv : the preprint server for biology · 2025Article
- Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.Cell reports · 2024Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Hyperexcitability has been suggested to contribute to motoneuron degeneration in amyotrophic lateral sclerosis (ALS). If this is so, and given that the physiological type of a motor unit determines the relative susceptibility of its motoneuron in ALS, then one would expect the most vulnerable motoneurons to display the strongest hyperexcitability prior to their degeneration, whereas the less vulnerable should display a moderate hyperexcitability, if any. We tested this hypothesis in vivo in two unrelated ALS mouse models by correlating the electrical properties of motoneurons with their physiological types, identified based on their motor unit contractile properties. We found that, far from being hyperexcitable, the most vulnerable motoneurons become unable to fire repetitively despite the fact that their neuromuscular junctions were still functional. Disease markers confirm that this loss of function is an early sign of degeneration. Our results indicate that intrinsic hyperexcitability is unlikely to be the cause of motoneuron degeneration.
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Registered trials
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.