Clostridium Botox Research Paper

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Introduction
Clostridium Botulinum is the bacteria from which Botox is derived from. It can be found in its inactive form in the natural environment, in things such as the forest, cultivated soils and the sediment of lakes and streams, also in the intestinal tracts of mammals and fish. Naturally occurring forms of this bacteria and spores are normally harmless. Problems only arise when the spores transform into vegetative cells and the cell population increases to the point where the bacteria Clostridium Botulinum begin producing the botulinum toxin, a deadly neurotoxin responsible for botulism.1 Botulinum A toxin is one of seven serotypes (A-G), these toxins are responsible for four recognised types of diseases including infant botulism, wound botulism and food-borne and adult intestinal colonization.2, 3 In all cases, the toxin which is a Zn2+ endopeptidase, acts by blocking cholinergic synapses by cleaving intracellular proteins responsible for the docking and fusion of synaptic vesicles to the plasma membrane.4 Despite its toxicity, botulinum toxins have been found to have great value as pharmaceutical agents and are used to treat numerous diseases
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Acetylcholine then binds to receptors on the muscle fibre membrane (sarcolemma) causing depolarisation. A wave of depolarisation travels down tubules (T system). T system depolarisation leads to Ca2+ release from stores in sarcoplasmic reticulum. Ca2+ binds to proteins in the muscle, which leads to contraction. Acetylcholinesterase in the gap rapidly breaks down acetylcholine so that contraction only occurs when impulses arrive continuously. As acetylcholine is able to diffuse into the synaptic cleft, the electrical impulse continues to be conducted by the muscle causing the action potential to

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