Botulinum toxin type A injected into the orbicularis oculi relieves blepharospasm. The molecular basis of this therapeutic effect is:

• A Blockade of voltage-gated sodium channels in the motor axon terminal
• B Competitive antagonism of nicotinic receptors at the motor end plate
• C Irreversible inhibition of acetylcholinesterase in the synaptic cleft
• D Proteolytic cleavage of SNARE proteins required for acetylcholine vesicle fusion ✓

Explanation

Botulinum toxin is internalised by cholinergic terminals and its light chain cleaves SNARE proteins such as SNAP-25, preventing fusion of acetylcholine vesicles with the presynaptic membrane and reducing transmitter release. Recovery requires sprouting of new terminals over weeks to months, explaining the duration of action. Cholinesterase inhibition would increase acetylcholine, and postsynaptic nicotinic blockade describes curare, not botulinum toxin.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.