AFTER repetitive stimulation, the membrane potential of nerve fibres is transiently increased. It has been suggested by Ritchie and Straub1 that this hyperpolarization could be explained on the basis of two assumptions: that the ionic pump responsible for the coupled efflux of sodium ions and influx of potassium ions2 becomes hyperactive following stimulation because of the raised intra-cellular sodium ion concentration3; that the extracellular space adjacent to the membrane is confined by a diffusional barrier. Following activity, the hyperactive pump would deplete the potassium in this space and thus raise the membrane potential of the nerve fibre above its resting level. A consequence of this hypothesis is that, in the absence of extracellular potassium, the sodium pump would be unable to lower the potassium concentration further and there would be no post-tetanic hyperpolarization, as Ritchie and Straub1 indeed found in mammalian C-fibres. On the other hand, an increased post-tetanic hyperpolarization in potassium-free solutions has since been reported both in the same fibres4 and in frog nodes of Ranvier5.