Characteristics of taurine release from cerebral cortex slices induced by sodium-deficient media.
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. Moreover, 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.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002540:Cerebral Cortex / Q000502:physiology*; D046508:Culture Techniques; D005110:Extracellular Space / Q000502:physiology; D007473:Ion Channels / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000502:physiology*; D009435:Synaptic Transmission; D013654:Taurine / Q000378:metabolism*
D007473:Ion Channels; D013654:Taurine; D012964:Sodium; D011188:Potassium; D002118:Calcium