Dreyer F, Schmitt A
Neurosci Lett. 1981 Nov 4;26(3):307-11. doi: 10.1016/0304-3940(81)90150-6.
The quantal transmitter release of tetanus (TeTx) and botulinum A (BoTx) toxin paralyzed mouse diaphragms was studied. The very low release probability could be enhanced by increasing the frequency of nerve stimulation to 50 Hz or by the application of 4-aminopyridine. In the BoTx-muscles the endplate potentials were strongly coupled to the stimuli with synaptic delays similar to unpoisoned terminals. In contrast, in the TeTx-muscles large variations in the delay of release of quanta in response to stimulation were observed. From these findings it is suggested that TeTx and BoTx act at different sites of the depolarization-transmitter release process.
研究了破伤风毒素(TeTx)和肉毒杆菌A毒素(BoTx)使小鼠膈肌麻痹时的量子递质释放情况。通过将神经刺激频率提高到50Hz或应用4-氨基吡啶,可以增强极低的释放概率。在BoTx作用的肌肉中,终板电位与刺激紧密耦合,突触延迟与未中毒的终末相似。相比之下,在TeTx作用的肌肉中,观察到量子释放延迟对刺激的反应有很大变化。从这些发现表明,TeTx和BoTx作用于去极化-递质释放过程的不同位点。