Tetanospasmin travels via the bloodstream to the peripheral nerve endings, where it is taken up by motor neurons and transported retrogradely to the spinal cord and brainstem. In the CNS, it binds to specific receptors on inhibitory neurons, preventing the release of neurotransmitters like gamma-aminobutyric acid (GABA) and glycine. This blockade results in a loss of inhibitory control over motor neurons, causing the characteristic muscle spasms and rigidity.
