Abstract
Taurine release from rat cerebral cortex slices as influenced by changes in sodium metabolism has been investigated. Superfusion of the slices with sodium deficient medium enhanced taurine release in a reversible manner. The enhancement was about 6 times greater than that induced by 50 mM potassium. Moveover, elevated potassium concentrations slightly decreased the enhancement produced by sodium-free medium. Omission of calcium ions increased the spontaneous efflux of taurine and diminished, but did not abolish, the release induced either by sodium-free or high-potassium medium. The changes in taurine release in the presence of calcium were parallel to the changes in concomitant calcium uptake. Sodium-deficient medium decreased the potassium content of the slices, indicating inhibition of the Na +, K +-ATPase. In agreement with this result, ouabain greatly increased the spontaneous efflux of taurine and eliminated the stimulation by sodium-free medium. The present results emphasize the importance of the resting-state sodium gradients for neural cells to retain high taurine concentrations. Thus, when the Na +, K +-ATPase activity is inhibited, a decrease in sodium gradients may lead to a redistribution of taurine between cytoplasmic and interstitial spaces. Such a mechanism would allow taurine to act as an unspecific modulator of neural membrane events.
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