Penner R, Neher E, Dreyer F
Nature. 1986;324(6092):76-8. doi: 10.1038/324076a0.
The clostridial neurotoxins tetanus and botulinum toxin type A are known to block transmitter release from nerve terminals, probably by interfering with some essential process controlling exocytosis after the entry of Ca2+ ions. Although exocytosis occurs in many secretory cells, these toxins show a high specificity for neurones and the secretory response of cultured bovine adrenal medullary cells is not inhibited by exposure to medium containing tetanus or botulinum toxin type A (although it is by botulinum toxin type D). Here we report that when tetanus toxin and botulinum neurotoxin type A are injected intracellularly into chromaffin cells they strongly inhibit secretion, as revealed by the measurement of cell capacitance. These results indicate that these toxins are normally ineffective in chromaffin cells because they are not bound and internalized, so do not reach their site of action. Furthermore, we have localized the secretion-blocking effects of the toxin to a fragment comprising the light chain covalently linked to part of the heavy chain, suggesting that this part of the molecule contains the active site.
已知梭菌神经毒素破伤风毒素和A型肉毒杆菌毒素可阻断神经末梢的递质释放,这可能是通过干扰Ca2+离子进入后控制胞吐作用的某些基本过程实现的。尽管胞吐作用发生在许多分泌细胞中,但这些毒素对神经元具有高度特异性,且暴露于含有破伤风毒素或A型肉毒杆菌毒素的培养基中时,培养的牛肾上腺髓质细胞的分泌反应并未受到抑制(尽管会被D型肉毒杆菌毒素抑制)。在此我们报告,当将破伤风毒素和A型肉毒杆菌神经毒素细胞内注射到嗜铬细胞中时,通过测量细胞电容发现它们会强烈抑制分泌。这些结果表明,这些毒素在嗜铬细胞中通常无效,因为它们未被结合和内化,因此无法到达其作用位点。此外,我们已将毒素的分泌阻断作用定位到一个片段,该片段由与重链部分共价连接的轻链组成,这表明该分子的这一部分包含活性位点。