ArticleNeurobiology of disease2007
Anti-ganglioside antibodies alter presynaptic release and calcium influx.
Article in Neurobiology of disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 52 citations in OpenAlex.
- Pyridostigmine Treatment for Pediatric Axonal Guillain-Barré Syndrome.Muscle & nerve · 2026Article
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Review
- Studying IndependentThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Toxemia in Human Naturally Acquired Botulism.Toxins · 2020Review
- Effects of IgG anti-GM1 monoclonal antibodies on neuromuscular transmission and calcium channel binding in rat neuromuscular junctions.Experimental and therapeutic medicine · 2015Article
- Neurophysiological and immunohistochemical studies of IgG anti-GM1 monoclonal antibody on neuromuscular transmission: effects in rat neuromuscular junctions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Article
- Article
- Anti-ganglioside antibody internalization attenuates motor nerve terminal injury in a mouse model of acute motor axonal neuropathy.The Journal of clinical investigation · 2012Article
- Novel anti-idiotype antibody therapy for lipooligosaccharide-induced experimental autoimmune neuritis: use relevant to Guillain-Barré syndrome.Journal of neuroscience research · 2010Article
- An update on pathobiologic roles of anti-glycan antibodies in Guillain-Barré syndrome.F1000 biology reports · 2010Article
- Pathophysiological actions of neuropathy-related anti-ganglioside antibodies at the neuromuscular junction.The Journal of physiology · 2009Review
- Antiganglioside antibodies and their pathophysiological effects on Guillain-Barré syndrome and related disorders--a review.Glycobiology · 2009Review
- Pathogenesis and treatment of immune-mediated neuropathies.Therapeutic advances in neurological disorders · 2009Article
- The neuropathic potential of anti-GM1 autoantibodies is regulated by the local glycolipid environment in mice.The Journal of clinical investigation · 2009Article
- Cav2.1 voltage-dependent Ca2+ channel current is inhibited by serum from select patients with Guillain-Barré syndrome.Neurochemical research · 2009Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Acute motor axonal neuropathy (AMAN) variant of Guillain-Barré syndrome is often associated with IgG anti-GM1 and -GD1a antibodies. The pathophysiological basis of antibody-mediated selective motor nerve dysfunction remains unclear. We investigated the effects of IgG anti-GM1 and -GD1a monoclonal antibodies (mAbs) on neuromuscular transmission and calcium influx in hemidiaphragm preparations and in cultured neurons, respectively, to elucidate mechanisms of Ab-mediated muscle weakness. Anti-GM1 and -GD1a mAbs depressed evoked quantal release to a significant yet different extent, without affecting postsynaptic currents. At equivalent concentrations, anti-GD1b, -GT1b, or sham mAbs did not affect neuromuscular transmission. At fourfold higher concentration, an anti-GD1b mAb (specificity described in immune sensory neuropathies) induced completely reversible blockade. In neuronal cultures, anti-GM1 and -GD1a mAbs significantly reduced depolarization-induced calcium influx. In conclusion, different anti-ganglioside mAbs induce distinct effects on presynaptic transmitter release by reducing calcium influx, suggesting that this is one mechanism of antibody-mediated muscle weakness in AMAN.
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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.