Enomoto K
Department of Physiology, Shimane Medical University, Izumo, Japan.
Eur J Pharmacol. 1988 Mar 1;147(2):209-15. doi: 10.1016/0014-2999(88)90779-0.
The effects of vesamicol (AH5183), a blocker of acetylcholine transport, on the voltage-clamped neuromuscular junction of the frog were studied. Vesamicol (15-30 microM) reduced the peak height of the ionophoretically applied acetylcholine-induced current. The amplitude of the evoked endplate current was also decreased in the presence of vesamicol (30 microM). The endplate current was reduced further when the nerve was tetanically stimulated. The reduction of the endplate current after tetanic stimulation in the presence of vesamicol was due to a decrease in the mean quantal content. The decay time constants of the evoked endplate current and the miniature endplate current were also decreased by vesamicol. It was concluded that vesamicol acts as a postsynaptic blocker at the endplate. This neurotoxin could also decrease the immediately available quanta in the presynaptic nerve terminal, but the mechanism of action of vesamicol on transmitter release remains obscure.
研究了乙酰胆碱转运阻滞剂维生霉素（AH5183）对青蛙电压钳制神经肌肉接头的影响。维生霉素（15 - 30微摩尔）降低了离子电泳施加乙酰胆碱诱导电流的峰值高度。在存在维生霉素（30微摩尔）的情况下，诱发终板电流的幅度也降低。当神经进行强直刺激时，终板电流进一步降低。在存在维生霉素的情况下强直刺激后终板电流的降低是由于平均量子含量的减少。维生霉素还降低了诱发终板电流和微小终板电流的衰减时间常数。得出的结论是，维生霉素在终板处起突触后阻滞剂的作用。这种神经毒素也可减少突触前神经末梢中即刻可用的量子，但维生霉素对递质释放的作用机制仍不清楚。
