ArticleNeurobiology of disease2016
An animal model of Miller Fisher syndrome: Mitochondrial hydrogen peroxide is produced by the autoimmune attack of nerve terminals and activates Schwann cells.
Article in Neurobiology of disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Revealing intracochlear microtrauma during cochlear implantation using optical coherence tomography and electrochemical sensing.Scientific reports · 2025Article
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- Beneficial Effect of Bee Venom and Its Major Components on Facial Nerve Injury Induced in Mice.Biomolecules · 2023Article
- Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor.Acta neuropathologica communications · 2022Article
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Article
- Real time imaging of intra-axonal calcium flux in an explant mouse model of axonal Guillain-Barré syndrome.Experimental neurology · 2022Article
- The SELENOT mimetic PSELT promotes nerve regeneration by increasing axonal myelination in a facial nerve injury model in female rats.Journal of neuroscience research · 2022Article
- Latrotoxin-Induced Neuromuscular Junction Degeneration Reveals Urocortin 2 as a Critical Contributor to Motor Axon Terminal Regeneration.International journal of molecular sciences · 2022Article
- Signals Orchestrating Peripheral Nerve Repair.Cells · 2020Review
- Correlations between microRNA-146a and immunoglobulin and inflammatory factors in Guillain-Barré syndrome.The Journal of international medical research · 2020Article
- A CXCR4 receptor agonist strongly stimulates axonal regeneration after damage.Annals of clinical and translational neurology · 2019Article
- An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals.Cells · 2019Article
- Hydrogen peroxide is a neuronal alarmin that triggers specific RNAs, local translation of Annexin A2, and cytoskeletal remodeling in Schwann cells.RNA (New York, N.Y.) · 2018Article
- Moving forward with the neuromuscular junction.Journal of neurochemistry · 2017Review
- Schwann cells are activated by ATP released from neurons in anDisease models & mechanisms · 2017Article
- Hello from the Other Side: How Autoantibodies Circumvent the Blood-Brain Barrier in Autoimmune Encephalitis.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The neuromuscular junction is a tripartite synapse composed of the presynaptic nerve terminal, the muscle and perisynaptic Schwann cells. Its functionality is essential for the execution of body movements and is compromised in a number of disorders, including Miller Fisher syndrome, a variant of Guillain-Barré syndrome: this autoimmune peripheral neuropathy is triggered by autoantibodies specific for the polysialogangliosides GQ1b and GT1a present in motor axon terminals, including those innervating ocular muscles, and in sensory neurons. Their binding to the presynaptic membrane activates the complement cascade, leading to a nerve degeneration that resembles that caused by some animal presynaptic neurotoxins. Here we have studied the intra- and inter-cellular signaling triggered by the binding and complement activation of a mouse monoclonal anti-GQ1b/GT1a antibody to primary cultures of spinal cord motor neurons and cerebellar granular neurons. We found that a membrane attack complex is rapidly assembled following antibody binding, leading to calcium accumulation, which affects mitochondrial functionality. Consequently, using fluorescent probes specific for mitochondrial hydrogen peroxide, we found that this reactive oxygen species is rapidly produced by mitochondria of damaged neurons, and that it triggers the activation of the MAP kinase pathway in Schwann cells. These results throw light on the molecular and cellular pathogenesis of Miller Fisher syndrome, and may well be relevant to other pathologies of the motor axon terminals, including some subtypes of the Guillain Barré syndrome.
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