How Botox Prevents Muscle Contraction
A muscle contraction Is triggered when an action potential travels down the axon of a motor neuron to the muscles. Neurotransmitters are chemicals that transmit signals across a synapse from one neuron to another neuron, muscle, or a gland.
Within the plasma membrane of the active axon terminal; there are proteins called T-SNAREs (target SNARS) and VSNARS (vesicular snars) which bind to form a SNARE complex.
In the synaptic vesicles, the protein is known as synaptobrevin2 and In the plasma membrane the proteins are known as Syntaxin1 and SNAP25. Syntaxin1 forms a complex with SNAP25. As the synaptic vesicle moves towards the plasma membrane, the synaptobrevin2 also becomes incorporated within this complex. This is known as a ‘trans core SNARE complex’.
As the proteins bind, the synaptic vesicle moves closer to the plasma membrane forming a readily releasable pool of vesicles that store the compound acetylcholine. Calcium ions are released through calcium channels which bind with the proteins allowing the trans core SNARE complex to bind further until they fuse to the plasma membrane and are released into the synaptic space until they reach the receptors on the post synaptic neuron. This triggers an action potential.
Botulinum toxin is composed of independent functional domains linked by disulphide bond. The N-terminal light chain (LC) is the enzymatic domain, and the heavy chain (HC) includes two independent domains, such as the translocation domain (HCT) and the receptor binding domain (HCR)’’ (Anon., n.d.)
Botulinum toxin is a single cell with a thick wall which has a heavy chain and a light chain. Botulinum toxin works by invading and binding to nerves cells. Within the cell membrane of the axon motor neuron there is lipid molecule known as a gangliaside or (GT1V), which the botulinum toxin heavy chain binds to. Once the botulinum toxin has binded to its target cell, the membrane of the nerve terminal begins to constrict and internalization of the bolulinum toxin occurs, a process called endocytosis. Once internalized, the proton concentration increases causing the PH to lower, which triggers an amino-terminal segment of the botulinum toxins heavy chain to form a pore in the vesicle membrane of the endocytic compartment and the disulphide bond of the botulinum toxin to be split. The light chain is then released which passes through the pore of the membrane into the cytosol where it very specifically cleaves the SNARE complex SNAP25, This prevents the transmission of acetylcholine to the receptor cell resulting in flaccid paralysis. The axon membrane remains depolarized and unable to trigger any action potential.
The return of muscle function occurs after 3 – 4 months due to the sprouting of new side branches called axonal collaterals from the presynaptic nerve endings at the neuromuscular junctions of the paralyzed muscles giving the muscle the ability to move again.
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