The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...

The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...

The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...

The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...

An analysis of SNAP-25 isoform sequences indicates that there is a highly conserved arginine residue (198 in vertebrates, 206 in the genus Drosophila) within the C-terminal region, which is cleaved by botulinum neurotoxin A, with consequent blockade of neuroexocytosis. The possibility that it may play an important role in the function of the neuroexocytosis machinery was tested at neuromuscular...

Plastic Surgery, the number of aesthetic procedures involving botulinum neurotoxin type A (BoNT-A) increased 3681% between 1997 and 2008. Almost 2.5 million procedures were performed using this neurotoxin last year, accounting for approximately 25% of all nonsurgical aesthetic procedures performed in 2008.1 Both aesthetic and therapeutic uses of this neurotoxin are likely to increase in the com...

This article reviews the current and most neurologic uses of botulinum neurotoxin type A (BoNT-A), beginning with relevant historical data, neurochemical mechanism at the neuromuscular junction. Current commercial preparations of BoNT-A are reviewed, as are immunologic issues relating to secondary failure of BoNT-A therapy. Clinical uses are summarized with an emphasis on controlled clinical tr...

Botulinal neurotoxin continues to be a concern in food safety. The molecular biology of botulinal neurotoxin gene expression in Clostridium botuli-num is poorly understood. In this study, the transcriptional and translational kinetics of expression of type A botulinal neurotoxin by C. botulinum type A strains Hall A, 62A, and NCTC 2916 were determined during 96 hours of growth. Strains were gro...

This paper reviews the current and most neurological (central nervous system, CNS) uses of the botulinum neurotoxin type A. The effect of these toxins at neuromuscular junction lends themselves to neurological diseases of muscle overactivity, particularly abnormalities of muscle control. There are seven serotypes of the toxin, each with a specific activity at the molecular level. Currently, ser...

This review presents a brief account of the most significant biological effects and clinical applications of botulinum neurotoxins, in a way comprehensive even for casual readers who are not familiar with the subject. The most toxic known substances in botulinum neurotoxins are polypeptides naturally synthesized by bacteria of the genus Clostridium. These polypeptides inhibit acetylcholine rele...