—Potassium transport was assessed within synaptic terminals isolated from cerebral cortices of rats which experienced one or two maximal electroshock (ES) convulsions daily. No significant change in endogenous K content was present after 2 consecutive days of ES‐seizures. However, K decreased 22 % and 41 % after 4 and 6 days of convulsions respectively. After 6 days, synaptosomes from ES rats were able to accumulate K to the same extent as controls and were inhibited by ouabain to an equivalent extent (50%). When these synaptosomes from ES rats were preloaded with high concentrations of K, K leaked out at an increased rate. When diphenylhydantoin (DPH) was administered intraperitoneally from the second to the sixth day of ES‐convulsions, the decrease in endogenous K induced by chronic convulsions was corrected. In ion‐free media or with 50 mM Na, DPH had no effects on the enhanced efflux of K observed in vitro after ES‐seizures. However, with high Na (50–100 mm) and low K (0.2–1 mm) DPH stimulated K uptake but did not affect the ouabain inhibition. Under conditions optimal for K uptake (50 mm Na and 10 mm K), DPH did not affect K accumulation but it prevented in vitro ouabain inhibition. Our results indicate that repeated ES‐convulsions decreased K content within isolated nerve terminals by enhancing its passive leakage. In vivo DPH prevented the effects of ES‐seizures by stimulating the Na‐K pump and not by directly blocking the K leak.
|Original language||English (US)|
|Number of pages||14|
|Journal||Journal of Neurochemistry|
|State||Published - Jul 1972|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience