Abstract
Publisher Summary This chapter discusses a study to analyze taurine exit from cerebral cortex slices stimulated by sodium-deficient medium. The aim of this study was to investigate the influence of sodium depletion from brain slices on the efflux of taurine, a putative neurotransmitter or modulator. Rat cerebral cortex slices preloaded in standard Krebs–Ringer–HEPES–glucose medium (pH 7.4) with [3H]taurine (10 μmol/l) were superfused in small oscillating glass chambers at 310 K under O2. The spontaneous efflux of taurine was greatly increased by sodium-free choline-substituted medium: after a 120-min superfusion in standard and sodium-free medium, about 70 and 15% of the initial taurine was left in slices, respectively. The introduction of sodium-free medium after superfusion with standard medium provoked an abrupt tenfold stimulation of taurine exit, while 50 mmol/l potassium only trebled the exit. It was concluded that the sodium ions may participate in the transport of taurine in a more complex way than earlier studies on influx have suggested.
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