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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Retention of cleaved synaptosome-associated protein of 25 kDa (SNAP-25) in neuromuscular junctions: a new hypothesis to explain persistence of botulinum A poisoning.
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Retention of cleaved synaptosome-associated protein of 25 kDa (SNAP-25) in neuromuscular junctions: a new hypothesis to explain persistence of botulinum A poisoning.

机译：在神经肌肉接头中保留25 kDa的裂解的突触体相关蛋白（SNAP-25）：一种新的假说来解释肉毒杆菌A中毒的持续存在。

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摘要

Botulinum neurotoxins can block neurotransmitter release for several months. The molecular mechanism of these toxins' action is known, but the persistence of neuromuscular paralysis that they cause is unexplained. At frog neuromuscular junctions, application of botulinum toxin type A caused paralysis and reduced the C-terminus immunoreactivity of SNAP-25, but not that of the remaining N-terminus fragment. Botulinum toxin type C caused paralysis and reduced syntaxin immunoreactivity without affecting that of SNAP-25. Co-application of botulinum A and C reduced syntaxin immunoreactivity, and that of both C and N termini of SNAP-25. Application of hydroxylamine to de-palmitoylate SNAP-25 resulted in a slight reduction of the immunoreactivity of SNAP-25 N terminus, while it had no effect on immunoreactivity of botulinum A cleaved SNAP-25. In contrast, application of hydroxylamine to nerve terminals where syntaxin had been cleaved by botulinum C caused a considerable reduction in SNAP-25 N-terminus immunoreactivity. Hence the retention of immunoreactive SNAP-25 at the neuromuscular junction depends on its interactions with syntaxin and plasma membrane. Persistence of cleaved SNAP-25 in nerve terminals may prevent insertion of new SNAP-25 molecules, thereby contributing to the longevity of botulinum A effects.
机译：肉毒杆菌神经毒素可以阻止神经递质释放数月。这些毒素作用的分子机制是已知的，但尚不能解释它们引起的神经肌肉麻痹的持续性。在青蛙神经肌肉接头处，使用A型肉毒杆菌毒素会导致麻痹，并降低SNAP-25的C末端免疫反应性，但不会降低其余N末端片段的C末端免疫反应性。 C型肉毒杆菌毒素可引起麻痹并降低语法免疫反应性，而不会影响SNAP-25。肉毒杆菌A和C的共同应用降低了syntaxin的免疫反应性，并降低了SNAP-25的C和N末端的语法。将羟胺用于去棕榈酸酯SNAP-25导致SNAP-25 N末端的免疫反应性略有降低，而对肉毒杆菌A裂解的SNAP-25的免疫反应性没有影响。相反，将羟胺应用于肉毒杆菌C裂解了语法素的神经末梢，导致SNAP-25 N末端免疫反应性大大降低。因此，免疫反应性SNAP-25在神经肌肉接头处的保留取决于其与语法蛋白和质膜的相互作用。裂解的SNAP-25在神经末梢的持续存在可能阻止新的SNAP-25分子的插入，从而延长了肉毒杆菌A效应的寿命。

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