Abstract: The purpose of this study was to establish whether excessive lactate production associated with local application of K+ is reflected at the extracellular level during or after the K+ challenge. Changes in extracellular lactate were continuously monitored by microdialysis coupled to on-line fluorimetric analysis. K+-induced changes in dialysate lactate were closely related to those of the direct current potential. High K+ evoked a large and sustained negative shift of direct current potential onto which were superimposed a variable number of transient peaks of further depolarisation. The initial negative shift in direct current potential was associated with a decrease in dialysate lactate, but after each transient depolarisation, the positive shift in direct current potential indicating cell repolarisation was associated with a marked increase in extracellular lactate. When repetitive transient depolarisations occurred during a stimulus, only a small increase after each depolarisation was observed. However, recordings consistently revealed a marked and rapid increase in extracellular lactate after the K+ stimulus. These data indicate that extracellular lactate mostly increased during periods of repolarisation. This suggests strongly that lactic acid transport out of brain cells may be impaired when their transmembrane ionic gradients are disrupted.