Smith D O
J Physiol. 1983 Mar;336:143-57. doi: 10.1113/jphysiol.1983.sp014573.
Changes in extracellular K+ levels were measured during repetitive stimulation of the excitor axon of the opener muscle of the crayfish walking leg. Mesaxon channels, through which K+ might diffuse away from the periaxonal ('Frankenhaeuser-Hodgkin') space, were examined in electron micrographs; they were seen every 2-10 micron along the axon, and their average (+/- S.D.) length and width were 3.0 (+/- 1.6) micron and 19.8 (+/- 8.9) nm, respectively. Intracellular recordings revealed a 40 ms after-depolarization following an action potential; this was attributed to elevated levels of extracellular K+. During stimulation at 50 Hz, this resulted in a depolarizing shift of the membrane potential between impulses; the average depolarization was 9.3 mV, which corresponds to a 4.3 mM increase in extracellular K+. Using K+-selective micro-electrodes, changes in extracellular K+ activity, delta aK, were measured at distances ranging from 10 to 50 micron from the axon; during 50 Hz stimulation, delta aK rose within 15 s to a maximum value of 1.1 mM which was maintained at a steady level in most preparations. Conduction failure occurred in several preparations after at least 90 s of stimulation; levels of delta aK were not abnormally high in these cases. Soaking the axon for at least 15 min in saline with extracellular K+ levels at least 18 mM above normal values was necessary to cause blockage in unstimulated nerves. Soaking the preparation for 30 min in 10(-3) M-ouabain resulted in a 48% increase in the maximum values of delta aK during 50 Hz stimulation. It is concluded that K+ accumulates extracellularly during axon stimulation and that the extent of this accumulation is reduced by active uptake mechanisms; however, this accumulation probably cannot directly block action potential conduction, for neither the magnitude nor the kinetics of K+ build-up approach values shown to reduce excitability.
在重复刺激小龙虾步行腿 opener 肌肉的兴奋性轴突过程中，测量了细胞外 K⁺ 水平的变化。在电子显微镜下检查了中轴突通道，K⁺ 可能通过这些通道从轴周（“Frankenhaeuser-Hodgkin”）间隙扩散出去；沿轴突每 2 - 10 微米可见这些通道，其平均（±标准差）长度和宽度分别为 3.0（±1.6）微米和 19.8（±8.9）纳米。细胞内记录显示动作电位后有 40 毫秒的去极化后电位；这归因于细胞外 K⁺ 水平升高。在 50 赫兹刺激期间，这导致冲动之间膜电位的去极化偏移；平均去极化幅度为 9.3 毫伏，这相当于细胞外 K⁺ 增加 4.3 毫摩尔。使用 K⁺ 选择性微电极，在距轴突 10 至 50 微米的距离处测量细胞外 K⁺ 活性的变化，即ΔaK；在 50 赫兹刺激期间，ΔaK 在 15 秒内升至最大值 1.1 毫摩尔，并在大多数标本中维持在稳定水平。在至少 90 秒的刺激后，几个标本出现传导阻滞；在这些情况下，ΔaK 水平并非异常高。将轴突在细胞外 K⁺ 水平比正常值至少高 18 毫摩尔的盐溶液中浸泡至少 15 分钟，才会导致未受刺激神经的传导阻滞。将标本在 ¹⁰⁻³ M 哇巴因中浸泡 30 分钟，会使 50 赫兹刺激期间ΔaK 的最大值增加 48%。得出的结论是，轴突刺激期间 K⁺ 在细胞外积累，并且这种积累的程度因主动摄取机制而降低；然而，这种积累可能无法直接阻断动作电位传导，因为 K⁺ 积累的幅度和动力学都未达到显示会降低兴奋性的值。
