Tetanus toxin specifically targets GABAergic inhibitory interneurons in the central nervous system. It blocks the release of inhibitory neurotransmitters like GABA and glycine by cleaving synaptobrevin, a protein essential for neurotransmitter vesicle fusion. This inhibition causes disinhibition of motor neurons, leading to uncontrolled muscle contractions and spasms characteristic of tetanus. The toxin does not directly affect cholinergic motor neurons or sensory neurons but acts upstream by disrupting inhibitory control, resulting in the characteristic rigidity and spasms seen in tetanus patients.

Reference: Harrison's Principles of Internal Medicine, Kasper et al., 20th Edition.