ArticleExperimental neurology2016
Altered terminal Schwann cell morphology precedes denervation in SOD1 mice.
Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 43 citations in OpenAlex.
- Pathology of general proprioception in a canine disease model of amyotrophic lateral sclerosis.Journal of the neurological sciences · 2026Article
- The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Review
- Origin, identity, and function of terminal Schwann cells.Trends in neurosciences · 2024Review
- Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024Review
- Pathomechanistic Networks of Motor System Injury in Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2024Review
- Response of terminal Schwann cells following volumetric muscle loss injury.Experimental neurology · 2023Article
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- TDP-43 dysregulation and neuromuscular junction disruption in amyotrophic lateral sclerosis.Translational neurodegeneration · 2022Review
- Peripheral glia diversity.Journal of anatomy · 2022Review
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Small junction, big problems: Neuromuscular junction pathology in mouse models of amyotrophic lateral sclerosis (ALS).Journal of anatomy · 2022Review
- Article
- Functional regeneration of the murine neuromuscular synapse relies on long-lasting morphological adaptations.BMC biology · 2022Article
- Progress in perisynaptic Schwann cell and neuromuscular junction research.Neural regeneration research · 2022Article
- Ultra-early amplitude decrement after repetitive nerve stimulation supports early neuromuscular junction injury in amyotrophic lateral sclerosis: a prospective cross-sectional study.Neural regeneration research · 2022Article
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Validation of terminal Schwann cell gene marker expression by fluorescent in situ hybridization using RNAscope.Neuroscience letters · 2022Article
- hiPSC-Derived Schwann Cells Influence Myogenic Differentiation in Neuromuscular Cocultures.Cells · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
In mice that express SOD1 mutations found in human motor neuron disease, degeneration begins in the periphery for reasons that remain unknown. At the neuromuscular junction (NMJ), terminal Schwann cells (TSCs) have an intimate relationship with motor terminals and are believed to help maintain the integrity of the motor terminal. Recent evidence indicates that TSCs in some SOD1 mice exhibit abnormal functional properties, but other aspects of possible TSC involvement remain unknown. In this study, an analysis of TSC morphology and number was performed in relation to NMJ innervation status in mice which express the G93A SOD1 mutation. At P30, all NMJs of the fast medial gastrocnemius (MG) muscle were fully innervated by a single motor axon but 50% of NMJs lacked TSC cell bodies and were instead covered by the processes of Schwann cells with cell bodies located on the preterminal axons. NMJs in P30 slow soleus muscles were also fully innervated by single motor axons and only 5% of NMJs lacked a TSC cell body. At P60, about 25% of MG NMJs were denervated and lacked labeling for TSCs while about 60% of innervated NMJs lacked TSC cell bodies. In contrast, 96% of P60 soleus NMJs were innervated while 9% of innervated NMJs lacked TSC cell bodies. The pattern of TSC abnormalities found at P30 thus correlates with the pattern of denervation found at P60. Evidence from mice that express the G85R SOD1 mutation indicate that TSC abnormalities are not unique for mice that express G93A SOD1 mutations. These results add to an emerging understanding that TSCs may play a role in motor terminal degeneration and denervation in animal models of motor neuron disease.
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