An excess of repeated contraction of the muscles involved in facial expressions results in the appearance of fine lines known as expression wrinkles.
Skeletal muscle contraction is controlled by impulses from the central nervous system via the Neuromuscular Junctions (NMJs). Neurons receive chemical signals that produce changes in the membrane potential (depolarisation). When depolarisation is large enough, it is converted into an action potential that spreads along the axons. Then, a Ca2+ influx triggers the fusion of secretory vesicles, filled with neurotransmitters, with the plasma membrane. This fusion is mediated by the concerted action of the SNARE protein family (syntaxin, VAMP and SNAP25) and Munc18-1 protein.1
Munc18-1 binds to syntaxin helping to initiate the assembly of the SNARE complex forcing the vesicle to move closer to the neuronal membrane for their fusion.1,2 Munc18-1 has been reported to initiate and act on the folding intermediates of SNARE to chaperone and stabilise its assembly.3 It is also thought to mediate vesicle docking and fusion and even shaping fusion pore kinetics.2
After the fusion, the Acetylcholine (ACh) neurotransmitter is released into the synapse, and it travels to the muscle membrane to associate with its clustered receptor (AChRs) and trigger the postsynaptic pathway. Clustering of AChR is induced by the proteoglycan agrin which binds to the transmembrane receptor LRP4 activating the muscle-specific kinase (MuSK) receptor that, together with AChR associated protein rapsyn, causes AChR clustering.4 Rapsyn also links AChRs to the utrophinassociated complex, which appears to be required for AChR stabilisation.5
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