Botox

4 key steps in the mechanism of action of Botox:

1. Toxin is bound to specific receptors on the presynaptic cell surface. This is mediated by the half of the heavy chain of the C-terminal (approx 30 minutes).

2. Internalization. This is an endocystic process that is energy-dependent receptor-mediated. The nerve cell’s plasma membrane invaginates around the toxin-receptor complex to form a vesicle inside the nerve terminal that contains toxin.

3. Translocation. The disulfide bond is cleaved, after internalization, releasing the 50-kDa light chain of the toxin molecule across the endocytic vesicle’s endosomal membrane into the the nerve terminal’s cytoplasm.

4. Blocking. The 50-kDa light chain of serotypes A and E inhibit acetylcholine release by cleaving a cytoplasmic protein (SNAP-25) required for the docking of acetylcholine vesicles on the inner side of the nerve terminal plasma membrane. Botulinum toxin type D is specific for VAMP/synaptobrevin. Botulinum toxin types B and F also affect the VAMP/synaptobrevin protein. These actions impede the release of acetylcholine into the synaptic cleft.