SUMMARY1. Changes in extracellular K+ levels were measured during repetitive stimulation of the excitor axon of the opener muscle of the crayfish walking leg.2. 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 jam along the axon, and their average (± S.D.) length and width were 3 0 (± 1-6) gsm and 19'8 (± 8 9) nm, respectively.3. 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+.4. Using K+-selective micro-electrodes, changes in extracellular K+ activity, AaK, were measured at distances ranging from 10 to 50 ,um from the axon; during 50 Hz stimulation, AaK rose within 15 s to a maximum value of 1 1 mm which was maintained at a steady level in most preparations.5. Conduction failure occurred in several preparations after at least 90 s of stimulation; levels of AaK were not abnormally high in these cases.6. 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.7. Soaking the preparation for 30 min in 10-3 M-ouabain resulted in a 48 % increase in the maximum values of AaK during 50 Hz stimulation.8. 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.