ArticleThe Journal of physiology2011
Altered postnatal maturation of electrical properties in spinal motoneurons in a mouse model of amyotrophic lateral sclerosis.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.
- State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model.Amyotrophic lateral sclerosis & frontotemporal degeneration · 2015Pooled it
- Flecainide in Amyotrophic Lateral Sclerosis as a Neuroprotective Strategy (FANS): A Randomized Placebo-Controlled Trial.EBioMedicine · 2015Trial
- Motor Cortex Hyperexcitability Is Coupled to Neuromuscular Dysfunction in Aged Mice.Aging cell · 2026Article
- Human iPSC-Derived Spinal Cord Organoids - The First Electrophysiological Assessment of Neuronal Maturation.ACS chemical neuroscience · 2026Article
- 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
- Riluzole treatment paradoxically increases motoneuron excitability in ALS due to hyperactive homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Article
- Modeling cerebral palsy in animals.Developmental medicine and child neurology · 2026Review
- SK channel upregulation and sex-specific mechanisms drive spinal motoneuron reduced excitability with age.Frontiers in aging neuroscience · 2026Article
- Article
- Review
- Trimetazidine stimulates intracellular CaScientific reports · 2025Article
- Age-related increase in the excitability of mouse layer V pyramidal neurons in the primary motor cortex is accompanied by an increased persistent inward current.GeroScience · 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
- How do we get from hyperexcitability to excitotoxicity in amyotrophic lateral sclerosis?Brain : a journal of neurology · 2024Review
- Intrinsic motoneuron properties in typical human development.The Journal of physiology · 2024Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Spinal motoneurons are highly vulnerable in amyotrophic lateral sclerosis (ALS).Previous research using a standard animal model, the mutant superoxide dismutase-1 (SOD1)mouse, has revealed deficits in many cellular properties throughout its lifespan. The electrical properties underlying motoneuron excitability are some of the earliest to change; starting at 1 week postnatal, persistent inward currents (PICs) mediated by Na+ are upregulated and electrical conductance, a measure of cell size, increases. However, during this period these properties and many others undergo large developmental changes which have not been fully analysed.Therefore, we undertook a systematic analysis of electrical properties in more than 100 normal and mutant SOD1 motoneurons from 0 to 12 days postnatal, the neonatal to juvenile period.We compared normal mice with the most severe SOD1 model, the G93A high-expressor line. We found that the Na+ PIC and the conductance increased during development. However, mutant SOD1 motoneurons showed much greater increases than normal motoneurons; the mean Na+PIC in SOD1 motoneurons was double that of wild-type motoneurons. Additionally, in mutant SOD1 motoneurons the PIC mediated by Ca2+ increased, spike width decreased and the time course of the after-spike after-hyperpolarization shortened. These changes were advances of the normal effects of maturation. Thus, our results show that the development of normal and mutant SOD1 motoneurons follows generally similar patterns, but that the rate of development is accelerated in the mutant SOD1 motoneurons. Statistical analysis of all measured properties indicates that approximately 55% of changes attributed to the G93A SOD1 mutation can be attributed to an increased rate of maturation.
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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.