Describe the mechanism of action of Botox (Botulinum toxin) including an account of the biochemical process that it inhibits. Include a diagram to illustrate your answer. PDF

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This is an essay to answer the 2018/19 question: Describe the mechanism of action of Botox (Botulinum toxin) including an account of the biochemical process that it inhibits. Include a diagram to illustrate your answer. including diagrams...

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Q. Describe the mechanism of action of Botox (Botulinum toxin) including an account of the biochemical process that it inhibits. Include a diagram to illustrate your answer. The botulinum toxin is a toxin produced by the anaerobic bacterium clostridium botulinum. It is known to cause food poisoning and paralysis. Botullinum neurotoxins have the ability to disrupt neurotransmission, this has been exploited for use in several medical applications. They are now the therapeutics of choice for the treatment of several neuromuscular conditions. The botulinum toxin structure consists of a heavy chain, which is involved of entry of the toxin into cells, and the light chain, which is involved in protease activity.

Botulinum neurotoxin has 7 serotypes, A – G. These botulinum neurotoxins, along with tetanus neurotoxin, which is produced by Clostridium tetani, make up the clostridial neurotoxin family. All of these CNTs have a similar fundamental mode of action, causing the inhibition of neurotransmission. They do so by a specific cleavage of a group of proteins integral to the exocytotic process, the SNARE proteins. The SNARE proteins function by (insert that bit here). The cleavage of one of these proteins would therefore result in a block of in the release of vesicular contents to the extracellular environment. Botulinum neurotoxin types B, D, F and G all cleave synaptobrevin, whilst types A, C and E all cleave SNAP25, type C also cleaves syntaxin. The botulinum toxin mechanism of action requires three discrete stages. It must first bind to the target cell so that it can internalise itself. It does so via its Hc binding domains. The second stage is translocation, this involves a structural rearrangement of the toxin within the cell under pH-dependant, acidic conditions. The third stage involves the inhibition of neurotransmitter release via the cleavage of SNARE proteins as it prevents the release of acetylcholine. The coupling between Ca2+ influx and fusion is disrupted....