INVESTIGATIONS carried out in our laboratory during the past three years have demonstrated that relatively small increases in potassium (K+) concentration in the cerebrospinal fluid (CSF) perfused over the dorsal hippocampus1 or neocortex2 can initiate seizure activity in these structures. A latent period of 15 to 40 minutes elapses between the beginning of the perfusion and the start of seizure activity, indicating the presence in the normal brain of probably functional barriers protecting neurons against K+ accumulation. Analysis of evoked responses3 and slow potential (DC) shifts4 during the period in which the epileptogenic phenomena are built up disclosed almost identical changes with those induced by rapid repetitive electrical epileptogenic stimulation of the same structures. These findings, along with data obtained by others,5-11 have led to the hypothesis that a localized increase of potassium in the extracellular spaces of the brain could be able to