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. 2015 Oct;4(5):543–554. doi: 10.3978/j.issn.2223-4683.2015.10.02

Figure 1.

Figure 1

BTA entry and mechanism of action. BTA binds with low affinity to polysialogangliosides on the surface of the cell, and with high affinity to synaptic vesicle protein SV2. After endocytosis, the light chain is cleaved and released into the cystosol, where it cleaves SNAP-25 thereby disrupting SNARE-dependent exocytosis of neurotransmitters and receptor trafficking to the plasma membrane. BTA decreases neurogenic inflammation by blocking NGF and neuropeptide (CGRP and SP) release from afferent nerves. It also disrupts receptor trafficking to the plasma membrane (TRPV1, P2X3). ATP, adenosine triphosphate; ACh, acetylcholine; CGRP, calcitonin gene-related peptide; SP, substance P; NGF, nerve growth factor; BTA, botulinum toxin A; SV2, synaptic vesicle protein 2.