Sodium outflux and influx within nerve terminals from chronic epileptogenic foci.

The Na+-pump (oMpNa) or maximal sodium outflux inhibited by ouabain was studied in nerve terminals isolated from the primary and mirror epileptogenic foci of freezing lesions. In addition, the Na+ for Na+ exchange diffusion that is sensitive to ethacrynic acid and furosemide was also analyzed. oMpNa in control and epileptogenic states had similar and indistinguishable activation curves for K0 (extracellular K) in a sodium medium except for a two-fold difference in magnitude. However, the apparent affinity of the Na+-pump for K0 as measured by K1/2 was shifted to the right or decreased in epileptogenic foci (2 mM K0 compared to 0.5 mM in controls) when measured in a magnesium medium. A decrease in the apparent affinity for internal sodium was also observed. Of the total sodium outflux (67.7 nmol/mg/min), Na+ movements which are insensitive to ouabain and external K+ but stimulated by external Na+ and inhibited by furosemide and ethacrynic acid (20 nmol/mg/min or 32% of sodium outflux) represented the Na+ for Na+ exchange diffusion in nerve terminals. Na+ influx rising with increasing internal sodium in the presence of ouabain and blocked by furosemide represent the corresponding inward Na+ movement. No differences were observed between controls and epileptogenic states.