Potent neurotoxins produced by Clostridium botulinum. Seven serologically distinct types are known, designated A-G; mol wt ≈150 kDa. Zinc-proteases synthesized as non-toxic single-chain precursors which become toxic upon proteolytic cleavage. Active form consists of one heavy and one light chain linked by a disulfide bond. Prevents release of acetylcholine from presynaptic nerve terminals at the neuromuscular junction. Identification of the causative agent of botulism: E. P. Van Ermengem, Z. Hyg. Infektionskrankh. 26, 1 (1897). Isoln: P. T. Snipe, H. Sommer, J. Infect. Dis. 43, 152 (1928). Review of isoln and purification: L. L. Simpson et al., Methods Enzymol. 165, 76-85 (1988); of structure and function: K. Oguma et al., Microbiol. Immunol. 39, 161-168 (1995). Review of pharmacology: J. L. Middlebrook, J. Toxicol. Toxin Rev. 5, 177-190 (1986); of mode of action and detection: M. Wictome, C. C. Shone, J. Appl. Microbiol. Symp. Suppl. 84, 87S-97S (1998). Review of clinical uses in focal dystonias: K. R. Kessler, R. Benecke, Neurotoxicology 18, 761-770 (1997); in cosmetic dermatology: A. Carruthers, J. Carruthers, Basic Clin. Dermatol. 15, 207-236 (1998).
Clinical trial in blepharospasm: B. Arthurs et al., Can. J. Ophthalmol. 22, 24 (1987); in achalasia: P. J. Pasricha et al., N. Engl. J. Med. 332, 774 (1995); in hyperhidrosis: M. Heckmann et al., ibid. 344, 488 (2001); in spasticity following stroke: A. Brashear et al., ibid. 347, 395 (2002).
Clinical trial in cervical dystonia: P. A. Cullis et al., Adv. Neurol. 78, 227 (1998).
Muscle relaxant (skeletal).
Muscle Relaxant (Skeletal)