ArticleNeurology international2009
Early detachment of neuromuscular junction proteins in ALS mice with SODG93A mutation.
Article in Neurology international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Characterization of the Contribution of Genetic Background and Gender to Disease Progression in the SOD1 G93A Mouse Model of Amyotrophic Lateral Sclerosis: A Meta-Analysis.Journal of neuromuscular diseasesPooled it
- Muscle-specific kinase levels in blood are an early diagnostic biomarker for SOD1-93A mouse model of ALS.Frontiers in neurology · 2025Article
- Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Small junction, big problems: Neuromuscular junction pathology in mouse models of amyotrophic lateral sclerosis (ALS).Journal of anatomy · 2022Review
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Central activation deficits contribute to post stroke lingual weakness in a rat model.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Protocatechuic Acid Extends Survival, Improves Motor Function, Diminishes Gliosis, and Sustains Neuromuscular Junctions in the hSOD1Nutrients · 2020Article
- Functional characterization of extrinsic tongue muscles in the Pink1-/- rat model of Parkinson disease.PloS one · 2020Article
- Bojungikgi-tang Improves Muscle and Spinal Cord Function in an Amyotrophic Lateral Sclerosis Model.Molecular neurobiology · 2019Article
- Neuromuscular Junction Morphology and Gene Dysregulation in the Wobbler Model of Spinal Neurodegeneration.Journal of molecular neuroscience : MN · 2018Article
- Sporadic amyotrophic lateral sclerosis (SALS) - skeletal muscle response to cerebrospinal fluid from SALS patients in a rat model.Disease models & mechanisms · 2018Article
- Neurotoxicity of the Cyanotoxin BMAA Through Axonal Degeneration and Intercellular Spreading.Neurotoxicity research · 2018Article
- Opposite Synaptic Alterations at the Neuromuscular Junction in an ALS Mouse Model: When Motor Units Matter.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2015Article
- Early changes of neuromuscular transmission in the SOD1(G93A) mice model of ALS start long before motor symptoms onset.PloS one · 2013Article
- Early gene expression changes in spinal cord from SOD1(G93A) Amyotrophic Lateral Sclerosis animal model.Frontiers in cellular neuroscience · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transgenic animals with mutant copper/zinc superoxide dismutase (SOD1) DNA develop paralytic motor neuron disease resembling human amyotrophic lateral sclerosis (ALS) patients and are commonly used as models for ALS. In the transgenic (Tg) mice with the G93A mutation of the human SOD1 gene SOD1(G93A) mice), the loss of ventral root axons and the synapses between the muscles and the motor neurons suggested that the motor neuron degeneration might proceed in a dying-back degeneration pattern. To reveal the relationship between axonal degeneration and the progression of the muscle atrophy in the SOD1(G93A) mice, we investigated the status of the neuromuscular junction along the disease progression. As a presynaptic or postsynaptic marker of neuromuscular junction (NMJ), anti-synaptic vesicle protein 2 (anti-SV2) antibody and α-bungarotoxin (α-BuTX) were chosen in this study and, as a marker of synaptic cleft, anti-agrin antibody was chosen in this study. In the immunohistochemistry of α-BuTX and anti-SV2 antibody, the percentages of double positive NMJs among α-BuTX single positive were decreased in Tg mice through time from ten weeks. The number of postsynaptic acethylcholine receptor (AChR) clusters did not decrease in Tg mice even at the end stage. Immunohistochemistry of α-BuTX and anti-agrin antibody revealed that the increase of immunopositive area of anti-agrin antibody around the muscle fiber in Tg mice from ten weeks of age. In this study, we revealed that the detachment of nerve terminals started at ten weeks in Tg mice. The levels of AChR did not change throughout 5-20 weeks of age in both groups of mice, and AChR remains clustering at NMJs, suggesting that the muscle abnormality is the result of detachment of nerve terminals.
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