Grossman Y, Gutnick M J
Brain Res. 1981 Apr 27;211(1):196-201. doi: 10.1016/0006-8993(81)90083-4.
In the metathoracic ganglion (T3) of the cockroach, extracellular potassium activity (aK) was measured with ion-sensitive microelectrodes and intracellular recordings were simultaneously made from giant axons (GAs) during high frequency stimulation of the connectives. Blockade of spike conduction through T3 was associated with intraganglionic aK rises of 0.2-0.5 mM, which were only 10% of the periaxonal aK rises suggested from GA depolarizations. When aK in the bath was increased 10-fold, GA conduction block during 1 Hz stimulation did not occur until much higher levels of aK and GA depolarization were achieved. The results suggest that glial sheaths surrounding GAs significantly impede K+ movement, and may thus prevent non-specific axonal interactions, and that stimulus-induced conduction block is not primarily due to K+-induced depolarization and consequent Na+-inactivation.
在蟑螂的后胸神经节(T3)中,用离子敏感微电极测量细胞外钾活性(aK),并在高频刺激连接体时,同时从巨轴突(GA)进行细胞内记录。通过T3的动作电位传导阻滞与神经节内aK升高0.2 - 0.5 mM有关,这仅为GA去极化所提示的轴突周围aK升高的10%。当浴液中的aK增加10倍时,在1 Hz刺激期间,直到达到更高水平的aK和GA去极化才会出现GA传导阻滞。结果表明,围绕GA的神经胶质鞘显著阻碍K + 移动,因此可能防止非特异性轴突相互作用,并且刺激诱导的传导阻滞主要不是由于K + 诱导的去极化和随之而来的Na + 失活。