Abstract

AbstractThe sodium and potassium contents of rat brain cortex slices incubated in bicarbonate medium were measured and the intracellular quantities estimated on the basis of the inulin distribution. Ethanol (109 mM) did not affect the ion content of unstimulated tissue during passive leakage in cold medium or aerobic incubation at 37o C.The effects of ethanol (109 mM), tert. butanol (34 mM) and clomethiazole (0.39 mM) were tested on the response to electrical stimulation (entry of sodium and loss of potassium in the non‐inulin space) as well as on the restoration of the ionic gradients occurring after a period of stimulation. All agents selectively inhibited the entry of sodium on stimulation with very little effect on potassium loss. The result is considered compatible with preferential action of the drugs on the activation step of the sodium channel controlling movement of sodium during the excitation cycle, and presumably located on the outside of the membranes. During recovery, no inhibition of sodium expulsion was observed, whereas both alcohols‐ but not clomethiazole‐slightly decreased the accumulation of potassium. Considered together with other observations, this finding suggests a special affinity of ethanol for the potassium binding site in the ion transport system.

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