Relation of spastic and flaccid paralysis to retrograde transport of 125I-tetanus toxin and its 125I-Ibc fragment. Modulating effect of F (ab) antibodies directed to specific areas on the toxin molecule.

The injection into mice of small doses of tetanus toxin induces spastic paralysis as is well-known, whereas large doses of toxin produce flaccid paralysis. The hypothesis has been put forward that the type of symptoms produced may depend on the axonal transport or the lack of axonal transport of the toxin molecule to the central nervous system. In the present paper we show that the lethal flaccid paralysis occurring in mice injected with a very large dose of toxin develops in the absence of any uptake and axonal transport of the toxin molecule. We also confirm that a tetanus toxin-derived fragment, the Ibc fragment, which is not transported retrogradely, produces flaccid paralysis. The blockage with the aid of specific antibody F(ab) fragments of the area on the toxin molecule which is involved in binding and axonal transport does prevent the toxin from being transported to the CNS and causes it to produce flaccid paralysis.