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Explain how tetanospasmin produces rigidity and spasms according to the material.
Answer
After inoculation and spore germination in an anaerobic environment, toxin is produced. Tetanospasmin migrates retrogradely along axons and inhibits inhibitory neurotransmitters, especially GABA and glycine. Inhibition is reduced, excitatory stimulation is exaggerated, and rigidity and spasms result.
Explanation
The expected explanation links the steps rather than merely naming the toxin: anaerobic germination permits toxin production; tetanospasmin travels by retrograde axonal migration; inhibitory neurotransmission involving **GABA** and **glycine** is blocked; and excitatory activity becomes relatively unopposed. The clinical result is rigidity and spasms. **Key takeaway:** Loss of inhibitory control explains the characteristic hyperexcitability.\n\n**Glossary:** **Retrograde axonal migration**: movement along a nerve toward the cell body; **neurotransmitter**: a chemical messenger between nerve cells.
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