Kryzhanovskiĭ G N, Polgar A A, Smirnova V S, Zinkevich V A
Biull Eksp Biol Med. 1985 Apr;99(4):407-9.
The effect of Ca2+ removal from the external medium on regulation of the release of the synaptic transmitter in the tetanus toxin (TT)-inhibited neuromuscular junctions was studied on a rat phrenicodiaphragmal preparation with the aid of the conventional microelectrode technique of recording synaptic activity. As the external concentration of calcium was decreased from 2 to 0 mM, the frequency of miniature end plate potentials remained unchanged in the preparations isolated 3 to 3.5 h after intramuscular injection of TT (10(5) MLD for mouse). TT considerably reduced activation of the transmitter release, caused in intact synapses by ouabain (0.1 mM) and repetitive stimulation of the diaphragmatic nerve (50 imp/s). The data obtained indicate that in the TT-inhibited motor nerve terminals, the level of the transmitter release does not depend on the external concentration of calcium and that TT damages some of the intracellular sources of calcium.
借助记录突触活动的传统微电极技术，在大鼠膈神经 - 膈肌标本上研究了从细胞外液中去除Ca²⁺对破伤风毒素（TT）抑制的神经肌肉接头处突触递质释放调节的影响。当细胞外钙浓度从2 mM降至0 mM时，在肌肉注射TT（小鼠10⁵最小致死量）后3至3.5小时分离的标本中，微小终板电位的频率保持不变。TT显著降低了哇巴因（0.1 mM）和膈神经重复刺激（50次/秒）在完整突触中引起的递质释放激活。所得数据表明，在TT抑制的运动神经末梢中，递质释放水平不依赖于细胞外钙浓度，并且TT损害了一些细胞内钙源。
