ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
Transynaptic Action of Botulinum Neurotoxin Type A at Central Cholinergic Boutons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Botulinum neurotoxin injections for muscle-based (dystonia and spasticity) and non-muscle-based (neuropathic pain) pain disorders: a meta-analytic study.Journal of neural transmission (Vienna, Austria : 1996) · 2020Pooled it
- Influence of botulinum toxin A in pain perception and condyle-fossa relationship after the management of temporomandibular dysfunction: a randomized controlled clinical trial.Oral and maxillofacial surgery · 2024Trial
- The Use of Botulinum Toxin in the Management of Headache Disorders.Handbook of experimental pharmacology · 2021Trial
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- Advances in Clostridial Neurotoxins: Passage of the Intestinal Barrier and Targeting of Specific Neuronal Cells.Toxins · 2026Review
- TTBK2-Driven Ciliogenesis Is Required for Intrinsic Neuronal Regeneration After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Botulinum Toxin: An Unconventional Tool for the Treatment of Depression?Brain sciences · 2025Review
- Botulinum Toxin Type A Exerts Direct Trans-Synaptic Action at Bilateral Spinal Nociceptive Circuits.Toxins · 2025Article
- Neurobiological mechanisms of botulinum neurotoxin-induced analgesia for neuropathic pain.Pharmacology & therapeutics · 2024Review
- Article
- Basis of movement control in dystonia and why botulinum toxin should influence it?Toxicon : official journal of the International Society on Toxinology · 2024Article
- Botulinum neurotoxin A modulates the axonal release of pathological tau in hippocampal neurons.Toxicon : official journal of the International Society on Toxinology · 2023Article
- Neurocircuitry underlying the antidepressant effect of retrograde facial botulinum toxin in mice.Cell & bioscience · 2023Article
- Intraoperative abobotulinumtoxinA alleviates pain after surgery and improves general wellness in a translational animal model.Scientific reports · 2022Article
- Lasting Peripheral and Central Effects of Botulinum Toxin Type A on Experimental Muscle Hypertonia in Rats.International journal of molecular sciences · 2022Article
- Toxicology and pharmacology of botulinum and tetanus neurotoxins: an update.Archives of toxicology · 2022Review
- Detection of VAMP Proteolysis by Tetanus and Botulinum Neurotoxin Type B In Vivo with a Cleavage-Specific Antibody.International journal of molecular sciences · 2022Article
- Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy.Toxins · 2021Review
- Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Botulinum neurotoxin Type A (BoNT/A) is an effective treatment for several movement disorders, including spasticity and dystonia. BoNT/A acts by cleaving synaptosomal-associated protein of 25 kDa (SNAP-25) at the neuromuscular junction, thus blocking synaptic transmission and weakening overactive muscles. However, not all the therapeutic benefits of the neurotoxin are explained by peripheral neuroparalysis, suggesting an action of BoNT/A on central circuits. Currently, the specific targets of BoNT/A central activity remain unclear. Here, we show that catalytically active BoNT/A is transported to the facial nucleus (FN) after injection into the nasolabial musculature of rats and mice. BoNT/A-mediated cleavage of SNAP-25 in the FN is prevented by intracerebroventricular delivery of antitoxin antibodies, demonstrating that BoNT/A physically leaves the motoneurons to enter second-order neurons. Analysis of intoxicated terminals within the FN shows that BoNT/A is transcytosed preferentially into cholinergic synapses. The cholinergic boutons containing cleaved SNAP-25 are associated with a larger size, suggesting impaired neuroexocytosis. Together, the present findings indicate a previously unrecognized source of reduced motoneuron drive after BoNT/A via blockade of central, excitatory cholinergic inputs. These data highlight the ability of BoNT/A to selectively target and modulate specific central circuits, with consequent impact on its therapeutic effectiveness in movement disorders.
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