Molgó J, Thesleff S
Brain Res. 1984 Apr 16;297(2):309-16. doi: 10.1016/0006-8993(84)90572-9.
In frogs poisoned with botulinum toxin type A the quantal content of endplate potentials is greatly reduced. Lowering the temperature of the preparation increases quantum content; between 14 and 4 degrees C the mean Q10 for this effect is 6.3. Facilitation of synaptic transmission is marked with pairs of stimuli and cooling further enhances facilitation. The time constant of decay of facilitation is 34 ms at 20 degrees C and 116 ms at 4 degrees C. The increase in facilitation and in its time constant of decay at low temperature are presumably not a result of a prolongation of the duration of the nerve terminal action potential since such changes are not seen in the presence of K+-channel blockade by 3,4-diaminopyridine. Electrotonic depolarization of nerve terminals in the presence of tetrodotoxin and 3,4-diaminopyridine induces all-or-none endplate currents. Such endplate currents, at a holding potential of -50 mV, show that the amount of charge entry is about 1/3 of that in unpoisoned junctions but still corresponds to 5-10 X 10(3) transmitter quanta. Transmitter release at this level is maintained during repetitive stimulation even in the presence of 82 mM Ca2+ in the extracellular solution. We speculate that the blockade of transmitter release in BoTx -poisoned muscles results from a stimulatory effect of the toxin on metabolic systems of Ca2+ disposal in the nerve terminal.
在用A型肉毒杆菌毒素中毒的青蛙中，终板电位的量子含量大大降低。降低标本温度会增加量子含量；在14至4摄氏度之间，这种效应的平均Q10为6.3。成对刺激时突触传递明显易化，冷却会进一步增强易化作用。在20摄氏度时易化衰减的时间常数为34毫秒，在4摄氏度时为116毫秒。低温下易化作用及其衰减时间常数的增加大概不是神经末梢动作电位持续时间延长的结果，因为在存在3,4 -二氨基吡啶对钾通道的阻断作用时未观察到这种变化。在存在河豚毒素和3,4 -二氨基吡啶的情况下，神经末梢的电紧张性去极化会诱发全或无的终板电流。在 - 50 mV的钳制电位下，这种终板电流表明电荷进入量约为未中毒接头的1/3，但仍相当于5 - 10×10³个递质量子。即使在细胞外溶液中存在82 mM Ca²⁺的情况下，在重复刺激期间这种水平的递质释放仍能维持。我们推测，肉毒杆菌毒素中毒肌肉中递质释放的阻断是由于毒素对神经末梢中Ca²⁺处理代谢系统的刺激作用所致。
