ArticlePhysiological reports2014
Soma size and Cav1.3 channel expression in vulnerable and resistant motoneuron populations of the SOD1G93A mouse model of ALS.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Riluzole treatment paradoxically increases motoneuron excitability in ALS due to hyperactive homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Article
- Dysregulation of persistent inward and outward currents in spinal motoneurons of symptomatic SOD1-G93A mice.The Journal of physiology · 2024Article
- Bifurcation analysis of motoneuronal excitability mechanisms under normal and ALS conditions.Frontiers in cellular neuroscience · 2023Article
- Motoneuron excitability dysfunction in ALS: Pseudo-mystery or authentic conundrum?The Journal of physiology · 2022Review
- Unique molecular features and cellular responses differentiate two populations of motor cortical layer 5b neurons in a preclinical model of ALS.Cell reports · 2022Article
- ALS-CSF-induced structural changes in spinal motor neurons of rat pups cause deficits in motor behaviour.Experimental brain research · 2021Article
- Shorter axon initial segments do not cause repetitive firing impairments in the adult presymptomatic G127X SOD-1 Amyotrophic Lateral Sclerosis mouse.Scientific reports · 2020Article
- Altered Motoneuron Properties Contribute to Motor Deficits in a Rabbit Hypoxia-Ischemia Model of Cerebral Palsy.Frontiers in cellular neuroscience · 2020Article
- Motor Neuron Susceptibility in ALS/FTD.Frontiers in neuroscience · 2019Review
- The vulnerability of spinal motoneurons and soma size plasticity in a mouse model of amyotrophic lateral sclerosis.The Journal of physiology · 2018Article
- Comparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons.Frontiers in cellular neuroscience · 2015Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Although the loss of motoneurons is an undisputed feature of amyotrophic lateral sclerosis (ALS) in man and in its animal models (SOD1 mutant mice), how the disease affects the size and excitability of motoneurons prior to their degeneration is not well understood. This study was designed to test the hypothesis that motoneurons in mutant SOD1(G93A) mice exhibit an enlargement of soma size (i.e., cross-sectional area) and an increase in Cav1.3 channel expression at postnatal day 30, well before the manifestation of physiological symptoms that typically occur at p90 (Chiu et al. 1995). We made measurements of spinal and hypoglossal motoneurons vulnerable to degeneration, as well as motoneurons in the oculomotor nucleus that are resistant to degeneration. Overall, we found that the somata of motoneurons in male SOD1(G93A) mutants were larger than those in wild-type transgenic males. When females were included in the two groups, significance was lost. Expression levels of the Cav1.3 channels were not differentiated by genotype, sex, or any interaction of the two. These results raise the intriguing possibility of an interaction between male sex steroid hormones and the SOD1 mutation in the etiopathogenesis of ALS.
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