The effects of electroshock seizures on potassium transport within synaptosomes from rat brain.

Abstract

Listen

Translate article

Abstract—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.