Baux G, Simonneau M, Tauc L
J Neurobiol. 1981 Jan;12(1):75-85. doi: 10.1002/neu.480120107.
The action of colchicine, a drug known to disrupt microtubules, on synaptic transmission and voltage-dependent phenomena was studied. Colchicine depressed transmission in both cholinergic and noncholinergic Aplysia ganglionic synapses. In some synapses, this effect was partly due to the curare like properties of the alkaloid. CA2+ currents, analyzed by voltage clamp techniques, were rapidly depressed by intracellular injection of colchicine and more slowly depressed by external application. Injected colchicine acted at much lower concentrations than required extracellularly. The implication of the reduced calcium influx in synaptic transmission is discussed. Colchicine caused a shift in the reversal potential of acetylcholine-activated chloride channels in a direction consistent with an increased intracellular chloride activity. It was concluded that the wide range of actions of colchicine on membrane properties should be taken into account when this drug is used in biological research.
研究了秋水仙碱(一种已知会破坏微管的药物)对突触传递和电压依赖性现象的作用。秋水仙碱抑制胆碱能和非胆碱能海兔神经节突触的传递。在某些突触中,这种作用部分归因于该生物碱类似箭毒的特性。通过电压钳技术分析的Ca2+电流,经细胞内注射秋水仙碱后迅速受到抑制,而经外部应用则抑制较慢。注射的秋水仙碱起作用所需的浓度远低于细胞外应用所需的浓度。讨论了钙内流减少在突触传递中的意义。秋水仙碱使乙酰胆碱激活的氯离子通道的反转电位发生偏移,其方向与细胞内氯离子活性增加一致。得出的结论是,在生物学研究中使用这种药物时,应考虑秋水仙碱对膜特性的广泛作用。