Related Experiment Video
Updated: Aug 17, 2026

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons
Published on: February 5, 2015
New insights into clostridial neurotoxin-SNARE interactions
Mark A Breidenbach1, Axel T Brunger
1Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.
Abstract:
Botulinum neurotoxin serotype A (BoNT/A) has achieved a dichotomous status in modern medicine; it is both a versatile treatment for several neurological disorders and a lethal poison responsible for causing the neuroparalytic syndrome botulism. The extent of paralysis largely depends on the dosage of toxin received. The toxins block neurotransmitter release by delivering their Zn(2+)-dependent protease components to the presynaptic side of chemical synapses. These highly specialized enzymes exclusively hydrolyze peptide bonds within SNARE (soluble N-ethylmaleiamide-sensitive factor attachment protein receptor) proteins. Recently, the structural basis for the highly specific interaction between BoNT/A and its target SNARE, SNAP-25 (synaptosomal-associated protein of 25kDa), was elucidated. New details regarding the nature of the toxin-SNARE interactions could be exploited for novel inhibitor design.
More Related Videos
Related Concept Videos
Botulism
Tetanus
Fusion of Secretory Vesicles with the Plasma Membrane
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
Ligand-Gated Ion Channel Receptor: Gating Mechanism

