Glavinović M I, Lee S, Miledi R
Department of Biophysics, University College London, U.K.
Neuroscience. 1989;31(1):181-6. doi: 10.1016/0306-4522(89)90039-0.
Miniature endplate potentials and currents were recorded from frog sartorius muscle fibres. As expected from previous work, La3+ caused a very large increase in miniature endplate potential frequency, followed by a progressive decrease, ending in the virtually complete disappearance of miniature endplate potentials. Soon after its application, La3+ caused an increase in the amplitude of miniature endplate potentials due to a lengthening of the underlying miniature endplate currents. Analysis of membrane current fluctuations produced by acetylcholine showed that La3+ caused an increase in the lifetime of the channels opened by acetylcholine. After miniature endplate potentials had vanished following La3+ treatment, the muscles were placed in organ culture conditions to see if miniature endplate potentials would reappear. After several hours miniature endplate potential activity was resumed in about 25% of the endplates, and disappeared again a few hours later, presumably because of accelerated nerve terminal degeneration. Preliminary electron microscopic observations suggest that the recovery of miniature endplate potential activity was accompanied by re-formation of synaptic vesicles in the motor endings.
从青蛙缝匠肌纤维记录微小终板电位和电流。正如先前工作所预期的,La3+ 使微小终板电位频率大幅增加,随后逐渐降低,最终微小终板电位几乎完全消失。在施加 La3+ 后不久,由于潜在微小终板电流延长,La3+ 使微小终板电位幅度增加。对乙酰胆碱产生的膜电流波动分析表明,La3+ 使乙酰胆碱开启的通道寿命增加。在 La3+ 处理后微小终板电位消失后,将肌肉置于器官培养条件下,观察微小终板电位是否会再次出现。数小时后,约25% 的终板恢复了微小终板电位活性,数小时后又再次消失,推测是由于神经末梢加速退化所致。初步电子显微镜观察表明,微小终板电位活性的恢复伴随着运动终末突触小泡的重新形成。