BOTULINUM TOXIN - MECHANISM OF PRESYNAPTIC BLOCKADE
BOTULINUM TOXIN - MECHANISM OF PRESYNAPTIC BLOCKADE
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DOI：
10.1126/science.785600
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发表时间：
1976-01-01
期刊：
影响因子：
56.9
通讯作者：
PRICE, DL
中科院分区：
文献类型：
--
作者：
KAO, I;DRACHMAN, DB;PRICE, DL
利用钙离子载体和黑寡妇蜘蛛毒液分析了肉毒杆菌毒素的作用机理。将钙离子载体添加到被肉毒杆菌毒素阻断的[小鼠]神经肌肉制剂中，并不增加微型终板电位的频率。这种蜘蛛毒液在被肉毒杆菌阻断后，引发了一连串的微型终板电位。用肉毒杆菌毒素处理的制剂的电子显微镜照片显示，在原本耗尽的神经末梢的释放部位，突触小泡聚集在一起。显然，肉毒杆菌毒素的作用不是由于囊泡中乙酰胆碱储存不足或阻止钙进入神经末梢，而是该毒素干扰了乙酰胆碱释放过程本身，可能是通过阻止释放部位的胞吐作用。
The mechanism of action of botulinum toxin was analyzed by the use of Ca ionophores and black widow spider venom. Addition of Ca ionophores to [mouse] nerve-muscle preparations blocked by botulinum toxin did not increase the frequency of miniature end plate potentials. The spider venom elicited a barrage of miniature end plate potentials after blockade by botulinum. Electron micrographs of preparations treated with botulinum toxin and then the spider venom revealed clumping of synaptic vesicles at release sites in the otherwise depleted nerve terminals. Apparently the action of botulinum toxin is not due to deficient storage of acetylcholine in vesicles or blockade of Ca entry into nerve terminals, but the toxin interferes with the acetylcholine release process itself, possibly by blocking exocytosis at the release sites.