ArticleInfection and immunity2012
Tetanus toxin and botulinum toxin a utilize unique mechanisms to enter neurons of the central nervous system.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 69 citations in OpenAlex.
- Structures of native SV2A reveal the binding mode for tetanus neurotoxin and anti-epileptic racetams.Nature communications · 2025Article
- Toxicology and pharmacology of botulinum and tetanus neurotoxins: an update.Archives of toxicology · 2022Review
- Synaptic Vesicle Glycoprotein 2A: Features and Functions.Frontiers in neuroscience · 2022Review
- Clostridial Neurotoxins: Structure, Function and Implications to Other Bacterial Toxins.Microorganisms · 2021Review
- Resolution of Two Steps in Botulinum Neurotoxin Serotype A1 Light Chain Localization to the Intracellular Plasma Membrane.International journal of molecular sciences · 2021Article
- Time-course transcriptomics reveals that amino acids catabolism plays a key role in toxinogenesis and morphology in Clostridium tetani.Journal of industrial microbiology & biotechnology · 2020Article
- Endocytosis, trafficking and exocytosis of intact full-length botulinum neurotoxin type a in cultured rat neurons.Neurotoxicology · 2020Article
- 4',6-Diamidino-2-Phenylindole Distinctly Labels Tau Deposits.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Article
- Protein Toxins That Utilize Gangliosides as Host Receptors.Progress in molecular biology and translational science · 2018Review
- Implications of Neuroinvasive Bacterial Peptides on Rodents Behaviour and Neurotransmission.Pathogens (Basel, Switzerland) · 2017Article
- Synthetic Cannabinoid-Induced Immunosuppression Augments Cerebellar Dysfunction in Tetanus-Toxin Treated Mice.Biomolecules & therapeutics · 2017Article
- Bacterial Signaling to the Nervous System through Toxins and Metabolites.Journal of molecular biology · 2017Review
- Entry of Botulinum Neurotoxin Subtypes A1 and A2 into Neurons.Infection and immunity · 2017Article
- A Novel Inhibitor Prevents the Peripheral Neuroparalysis of Botulinum Neurotoxins.Scientific reports · 2015Article
- Article
- A Heterologous Reporter Defines the Role of the Tetanus Toxin Interchain Disulfide in Light-Chain Translocation.Infection and immunity · 2015Article
- Accelerated intoxication of GABAergic synapses by botulinum neurotoxin A disinhibits stem cell-derived neuron networks prior to network silencing.Frontiers in cellular neuroscience · 2015Article
- Botulinum neurotoxin type A inhibits synaptic vesicle 2 expression in breast cancer cell lines.International journal of clinical and experimental pathology · 2015Article
- Effect of botulinum neurotoxin type A (BoNTA) on the morphology and viability of 3T3 murine fibroblasts.International journal of clinical and experimental pathology · 2015Article
- Botulinum Neurotoxins Can Enter Cultured Neurons Independent of Synaptic Vesicle Recycling.PloS one · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Botulinum neurotoxins (BoNTs) and tetanus neurotoxin (TeNT) are the most toxic proteins for humans. While BoNTs cause flaccid paralysis, TeNT causes spastic paralysis. Characterized BoNT serotypes enter neurons upon binding dual receptors, a ganglioside and a neuron-specific protein, either synaptic vesicle protein 2 (SV2) or synaptotagmin, while TeNT enters upon binding gangliosides as dual receptors. Recently, TeNT was reported to enter central nervous system (CNS) neurons upon synaptic vesicle cycling that was mediated by the direct binding to SV2, implying that TeNT and BoNT utilize common mechanisms to enter CNS neurons. This prompted an assessment of TeNT entry into CNS neurons, using the prototypic BoNT serotype A as a reference for SV2-mediated entry into synaptic vesicles, analyzing the heavy-chain receptor binding domain (HCR) of each toxin. Synaptic vesicle cycling stimulated the entry of HCR/A into neurons, while HCR/T entered neurons with similar levels of efficiency in depolarized and nondepolarized neurons. ImageJ analysis identified two populations of cell-associated HCR/T in synaptic vesicle cycling neurons, a major population which segregated from HCR/A and a minor population which colocalized with HCR/A. HCR/T did not inhibit HCR/A entry into neurons in competition experiments and did not bind SV2, the protein receptor for BoNT/A. Intoxication experiments showed that TeNT efficiently cleaved VAMP2 in depolarized neurons and neurons blocked for synaptic vesicle cycling. These experiments demonstrate that TeNT enters neurons by two pathways, one independent of stimulated synaptic vesicle cycling and one by synaptic vesicles independent of SV2, showing that TeNT and BoNT/A enter neurons by unique mechanisms.
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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.