Clostridium tetani produces tetanospasmin which causes spastic paralysis. What is the precise molecular mechanism of action of tetanospasmin at the level of inhibitory interneurons?

• A Cleaves synaptobrevin (VAMP) in inhibitory Renshaw cells, blocking glycine and GABA release ✓
• B Inhibits acetylcholine release at neuromuscular junction by cleaving SNAP-25
• C Activates voltage-gated sodium channels in motor neurons causing continuous firing
• D Blocks acetylcholinesterase at the neuromuscular junction

Explanation

Tetanospasmin is a zinc metalloprotease that cleaves synaptobrevin (VAMP-2), a SNARE protein essential for neurotransmitter vesicle fusion, specifically in glycinergic and GABAergic inhibitory interneurons (Renshaw cells). This prevents release of inhibitory neurotransmitters (glycine and GABA), leading to uncontrolled motor neuron firing and spastic paralysis. Botulinum toxin A/E cleaves SNAP-25 at the NMJ causing flaccid paralysis. Tetanospasmin does not block acetylcholinesterase or activate sodium channels.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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