Botulinum Toxin as a Pain Killer: Players and Actions in Antinociception
AbstractBotulinum neurotoxins (BoNTs) have been widely used to treat a variety of clinical ailments associated with pain. The inhibitory action of BoNTs on synaptic vesicle fusion blocks the releases of various pain-modulating neurotransmitters, including glutamate, substance P (SP), and calcitonin gene-related peptide (CGRP), as well as the addition of pain-sensing transmembrane receptors such as transient receptor potential (TRP) to neuronal plasma membrane. In addition, growing evidence suggests that the analgesic and anti-inflammatory effects of BoNTs are mediated through various molecular pathways. Recent studies have revealed that the detailed structural bases of BoNTs interact with their cellular receptors and SNAREs. In this review, we discuss the molecular and cellular mechanisms related to the efficacy of BoNTs in alleviating human pain and insights on engineering the toxins to extend therapeutic interventions related to nociception. View Full-Text
Share & Cite This Article
Kim, D.-W.; Lee, S.-K.; Ahnn, J. Botulinum Toxin as a Pain Killer: Players and Actions in Antinociception. Toxins 2015, 7, 2435-2453.
Kim D-W, Lee S-K, Ahnn J. Botulinum Toxin as a Pain Killer: Players and Actions in Antinociception. Toxins. 2015; 7(7):2435-2453.Chicago/Turabian Style
Kim, Dong-Wan; Lee, Sun-Kyung; Ahnn, Joohong. 2015. "Botulinum Toxin as a Pain Killer: Players and Actions in Antinociception." Toxins 7, no. 7: 2435-2453.