ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Early and persistent abnormal decoding by glial cells at the neuromuscular junction in an ALS model.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 96 citations in OpenAlex.
- Using human 3D organoid models to gain mechanistic insight in motor neuron diseases.Nature reviews. Neuroscience · 2026Review
- The evidence for old age motor neuron death: A scoping review.Physiological reports · 2026Article
- Neuromuscular junction innervation and motor function are preserved by restoring muscarinic signaling in perisynaptic glia in ALS.iScience · 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
- From inflammatory signaling to neuronal damage: Exploring NLR inflammasomes in ageing neurological disorders.Heliyon · 2024Review
- Origin, identity, and function of terminal Schwann cells.Trends in neurosciences · 2024Review
- Dietary NMN supplementation enhances motor and NMJ function in ALS.Experimental neurology · 2024Article
- Cellular and molecular evidence that synaptic Schwann cells contribute to aging of mouse neuromuscular junctions.Aging cell · 2023Article
- Response of terminal Schwann cells following volumetric muscle loss injury.Experimental neurology · 2023Article
- Early Alterations in Structural and Functional Properties in the Neuromuscular Junctions of Mutant FUS Mice.International journal of molecular sciences · 2023Article
- TDP-43 dysregulation and neuromuscular junction disruption in amyotrophic lateral sclerosis.Translational neurodegeneration · 2022Review
- Small junction, big problems: Neuromuscular junction pathology in mouse models of amyotrophic lateral sclerosis (ALS).Journal of anatomy · 2022Review
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Progress in perisynaptic Schwann cell and neuromuscular junction research.Neural regeneration research · 2022Article
- Phosphorylated TDP-43 aggregates in peripheral motor nerves of patients with amyotrophic lateral sclerosis.Brain : a journal of neurology · 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
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a late-onset neuromuscular disease characterized by progressive loss of motor neurons (MNs) preceded by neuromuscular junction (NMJ) denervation. Despite the importance of NMJ denervation in ALS, the mechanisms involved remain unexplored and ill defined. The contribution of glial cells in the disease has been highlighted, including axonal Schwann cell activation that precedes the decline of motor function and the onset of hindlimb paralysis. Because NMJ denervation occurs early in the process and that perisynaptic Schwann cells (PSCs), glial cells at the NMJ, regulate morphological stability, integrity, and repair of the NMJ, one could predict that PSC functions would be altered even before denervation, contributing to NMJ malfunctions. We tested this possibility using a slowly progressive model of ALS (SOD1(G37R) mice). We observed a normal NMJ organization at a presymptomatic stage of ALS (120 d), but PSC detection of endogenous synaptic activity revealed by intracellular Ca(2+) changes was enhanced compared with their wild-type littermates. This inappropriate PSC decoding ability was associated with an increased level of neurotransmitter release and dependent on intrinsic glial properties related to enhanced muscarinic receptor activation. The alteration of PSC muscarinic receptor functions also persists during the preonset stage of the disease and became dependent on MN vulnerability with age. Together, these results suggest that PSC properties are altered in the disease process in a manner that would be detrimental for NMJ repair. The impairments of PSC functions may contribute to NMJ dysfunction and ALS pathogenesis.
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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.