Botulinum toxin produces paralysis by acting at the neuromuscular junction. Its molecular target is:

• A Postsynaptic nicotinic acetylcholine receptors
• B SNARE proteins required for vesicle fusion ✓
• C Voltage-gated calcium channels on the nerve terminal
• D Acetylcholinesterase in the synaptic cleft

Explanation

Botulinum toxin is a zinc-dependent endopeptidase that cleaves SNARE proteins such as SNAP-25, syntaxin, and synaptobrevin, preventing docking and fusion of acetylcholine vesicles with the presynaptic membrane. Postsynaptic receptor destruction defines myasthenia gravis, cholinesterase inhibition defines organophosphate poisoning, and calcium channel antibodies define Lambert-Eaton myasthenic syndrome, making those mechanisms the key distractors to exclude.

Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.