{'fraction_non_alphanumeric': 0.037567968363816116, 'fraction_numerical': 0.022244191794364803, 'mean_word_length': 5.059880239520958, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Extracellular potassium levels and axon excitability during repetitive action potentials in crayfish.

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.