The freezing lesion. II. Potassium transport within nerve terminals isolated from epileptogenic foci

Abstract The generation of electrocorticographic seizures in freezing lesions was correlated with the ability of isolated synaptic terminals to actively transport potassium in vitro . Potassium content of synaptosomes from epileptogenic lesions was not significantly different from controls. However, when synaptosomes were incubated in Tris media, total K uptake decreased 59% while ouabain inhibition dropped 48% in the primary foci. In the mirror foci total K accumulation and ouabain inhibition both decreased 39%. Synaptosome K transport decreased more in the primary foci and in 6 of 13 experiments K appeared to be leaking out rather than going into synaptosomes. In order to rule out the effects of neuronal injury, studies were performed of non-epileptogenic lesions. Ouabain inhibition was not significantly changed while total K accumulation decreased 28%. These results show that an impairment in the synaptosome (Na+K) pump is intimately associated with the generation of seizures in primary and mirror foci. In addition, they suggest that synaptosome K leakage may be enhanced in lesion sites because: (1) in synaptosomes from inactive lesions total K uptake dropped without changes in ouabain inhibition and (2) in epileptogenic primary sites total K uptake decreased more than ouabain inhibition.