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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.