ArticleProceedings of the National Academy of Sciences of the United States of America2011
Physiological characterization of human muscle acetylcholine receptors from ALS patients.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03618966 (Neuromuscular Magnetic Stimulation Counteracts Muscle Decline in ALS Patients), which is not on this map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neuromuscular Magnetic Stimulation Counteracts Muscle Decline in ALS Patients
Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Neuromuscular magnetic stimulation counteracts muscle decline in ALS patients: results of a randomized, double-blind, controlled study.Scientific reports · 2019Trial
- Acetylcholine receptors from human muscle as pharmacological targets for ALS therapy.Proceedings of the National Academy of Sciences of the United States of America · 2016Trial
- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
- The Disruption of NMDAR/TRPM4 Death Signaling with TwinF Interface Inhibitors: A New Pharmacological Principle for Neuroprotection.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Review
- Classical and Unexpected Effects of Ultra-Micronized PEA in Neuromuscular Function.Biomolecules · 2022Review
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Effects of 3,4-diaminopyridine on myasthenia gravis: Preliminary results of an open-label study.Frontiers in pharmacology · 2022Article
- Creating stem cell-derived neuromuscular junctions in vitro.Muscle & nerve · 2021Review
- Imaging in vivo acetylcholine release in the peripheral nervous system with a fluorescent nanosensor.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Observational
- Using Xenopus oocytes in neurological disease drug discovery.Expert opinion on drug discovery · 2020Review
- Distinct Target-Specific Mechanisms Homeostatically Stabilize Transmission at Pre- and Post-synaptic Compartments.Frontiers in cellular neuroscience · 2020Article
- A Screen for Synaptic Growth Mutants Reveals Mechanisms That Stabilize Synaptic Strength.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Neuromuscular Junction Dismantling in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2017Review
- The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis.Brain pathology (Zurich, Switzerland) · 2016Review
- Generation of Functional Neuromuscular Junctions from Human Pluripotent Stem Cell Lines.Frontiers in cellular neuroscience · 2015Article
- Advances in cellular models to explore the pathophysiology of amyotrophic lateral sclerosis.Molecular neurobiology · 2014Review
- Partial block by riluzole of muscle sodium channels in myotubes from amyotrophic lateral sclerosis patients.Neurology research international · 2014Article
- In vitro Differentiation of Functional Human Skeletal Myotubes in a Defined System.Biomaterials science · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is characterized by progressive degeneration of motor neurons leading to muscle paralysis. Research in transgenic mice suggests that the muscle actively contributes to the disease onset, but such studies are difficult to pursue in humans and in vitro models would represent a good starting point. In this work we show that tiny amounts of muscle from ALS or from control denervated muscle, obtained by needle biopsy, are amenable to functional characterization by two different technical approaches: "microtransplantation" of muscle membranes into Xenopus oocytes and culture of myogenic satellite cells. Acetylcholine (ACh)-evoked currents and unitary events were characterized in oocytes and multinucleated myotubes. We found that ALS acetylcholine receptors (AChRs) retain their native physiological characteristics, being activated by ACh and nicotine and blocked by α-bungarotoxin (α-BuTX), d-tubocurarine (dTC), and galantamine. The reversal potential of ACh-evoked currents and the unitary channel behavior were also typical of normal muscle AChRs. Interestingly, in oocytes injected with muscle membranes derived from ALS patients, the AChRs showed a significant decrease in ACh affinity, compared with denervated controls. Finally, riluzole, the only drug currently used against ALS, reduced, in a dose-dependent manner, the ACh-evoked currents, indicating that its action remains to be fully characterized. The two methods described here will be important tools for elucidating the role of muscle in ALS pathogenesis and for developing drugs to counter the effects of this disease.
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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.