Mechanism of Action of Botox: A Cellular Perspective

Cell Biology
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Mechanism of action of Botox: Bacterium Clostridium botulinum and related species produce
Botulinum toxin (Botox) which is a neurotoxic protein. Botox exhibits its action by
preventing release of neurotransmitter acetylcholine at the axon endings which are present at
the neuromuscular junction. It led to flaccid paralysis. Botox is useful in the disorders like
overactive muscle movement, refractory overactive bladder, improper eye alignment,
migraine and neuropathic pain (Pirazzini, Rossetto, Eleopra, and Montecucco 2017).
Cell biology: It cleaves key proteins necessary for nerve activation. Botox binds to the nerves
which use acetylcholine. After binding of botox at the nerve terminal, it is taken by neuron in
the vesicles. With the movement of the vesicles further into the cell, acidification of vesicles
occurs. It results in pushing toxin across entire vesicle membrane and cytoplasm. After
entering into the cytoplasm, botox exhibits its action by cleaving soluble N-ethylmaleimide
sensitive factor attachment protein receptor (SNARE) protein. It averts release of
acetylcholine from the vesicles which results in halt in the nerve signalling and consequently
paralysis (Harper et al., 2014).
Released toxin from the bacterium comprises of single chain. It becomes activated when its
own proteases cleave it. After activation it produces two chains like heavy chain and light
chain which are responsible for its action. Heavy chain is responsible for binding to
presynaptic nerve terminals and translocation of light chain into the cell cytoplasm after
acidification of the vesicle acidification. Light chain is zinc metalloprotease which is
responsible for cleaving SNAP-25 member of SNARE protein family. Cleaved SNAP-25 is
responsible for the prevention of fusion of vesicles and cell membrane. It results in the
prevention of release of acetylcholine from the axon endings (Arsenault et al., 2014).
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