ArticleeNeuro
Time Course of Alterations in Adult Spinal Motoneuron Properties in the SOD1(G93A) Mouse Model of ALS.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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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
18 citing papers in PubMed, 27 citations in OpenAlex.
- 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
- Riluzole treatment paradoxically increases motoneuron excitability in ALS due to hyperactive homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Modeling cerebral palsy in animals.Developmental medicine and child neurology · 2026Review
- TDP-43 pathology is sufficient to drive axon initial segment plasticity and hyperexcitability of spinal motoneurones in vivo in the TDP43-ΔNLS model of Amyotrophic Lateral Sclerosis.Acta neuropathologica communications · 2025Article
- Restoring Homeostasis: Treating Amyotrophic Lateral Sclerosis by Resolving Dynamic Regulatory Instability.International journal of molecular sciences · 2025Article
- Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.Cell reports · 2024Article
- Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.bioRxiv : the preprint server for biology · 2024Article
- Dysregulation of persistent inward and outward currents in spinal motoneurons of symptomatic SOD1-G93A mice.The Journal of physiology · 2024Article
- Intrinsic motoneuron properties in typical human development.The Journal of physiology · 2024Article
- PICking out progressive PIC alterations in amyotrophic lateral sclerosis.Journal of neurophysiology · 2024Article
- Potential contribution of spinal interneurons to the etiopathogenesis of amyotrophic lateral sclerosis.Frontiers in neuroscience · 2024Review
- Inhibitory interneurons show early dysfunction in a SOD1 mouse model of amyotrophic lateral sclerosis.The Journal of physiology · 2023Article
- Motoneuron excitability dysfunction in ALS: Pseudo-mystery or authentic conundrum?The Journal of physiology · 2022Review
- Non-Invasive Transcutaneous Spinal DC Stimulation as a Neurorehabilitation ALS Therapy in Awake G93A Mice: The First Step to Clinical Translation.Bioengineering (Basel, Switzerland) · 2022Article
- Article
- Comparing therapeutic modulators of the SOD1 G93A Amyotrophic Lateral Sclerosis mouse pathophysiology.Frontiers in neuroscience · 2022Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
Although amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease, motoneuron electrical properties are already altered during embryonic development. Motoneurons must therefore exhibit a remarkable capacity for homeostatic regulation to maintain a normal motor output for most of the life of the patient. In the present article, we demonstrate how maintaining homeostasis could come at a very high cost. We studied the excitability of spinal motoneurons from young adult SOD1(G93A) mice to end-stage. Initially, homeostasis is highly successful in maintaining their overall excitability. This initial success, however, is achieved by pushing some cells far above the normal range of passive and active conductances. As the disease progresses, both passive and active conductances shrink below normal values in the surviving cells. This shrinkage may thus promote survival, implying the previously large values contribute to degeneration. These results support the hypothesis that motoneuronal homeostasis may be "hypervigilant" in ALS and a source of accumulating stress.
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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.