Most of the general aspects of the action of clostridial neurotoxin have been established using neuromuscular junction preparations as experimental model systems (Habermann and Dreyer, 1986). The neuromuscular endplate is the principal target in the "natural" poisoning process of botulinum neurotoxins. As little as 0.1 nM of BoNT/A is sufficient to completely block acetylcholine release within 90min (Dolly et a/., 1984; Gansel et a/., 1987). With TeTx, higher concentrations are required to achieve the same result (Dreyer, 1989). Several different neuromuscular junction preparations have been used, such as mouse hemidiaphragm, the levator auris longus muscle, the triangularis sterni nerve-muscle of mice, or the extensor digitorum longus muscle from rat. The mouse hemidiaphragm preparation is one of the most widely used systems. Inhibition of transmitter release can be conveniently monitored by recording from the muscle fiber or by measuring the strength of contraction. Furthermore, studies were also performed on frog neuromuscular junctions (Molgo and Thesleff, 1984) since they are easily accessible and can be used for long term experiments (Molgo etal., 1987).
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