Taurine and GABA release from mouse cerebral cortex slices: potassium stimulation releases more taurine than GABA...

The release of exogenous taurine and gamma-aminobutyric acid (GABA) was studied with slices from the developing mouse cerebral cortex. The spontaneous efflux of GABA increased with the cerebral GABA content during postnatal development, while the spontaneous efflux of taurine was approximately the same in both neonate and adult mice, in spite of a several-fold higher cerebral taurine content in the former. GABA, taurine and their structural analogues caused marked homo- and hetero-trans-stimulation of the release in both adult and developing mice, probably via membrane transport sites. The release was greatly enhanced by both 0.01 mM veratridine and exposure to sodium-free medium, the effects being more pronounced with GABA in the adults and with taurine in the neonates. The excitatory amino acids homocysteate, aspartate and kainate enhanced taurine release particularly from the developing cerebral cortex but were not effective on GABA release in the adults. The potassium stimulation of taurine release had a strikingly slow time course in both adult and developing mice. The responses in GABA release were also fairly slow in the neonates. Potassium stimulation evoked a large release of GABA in adult but not in developing mice. The evoked taurine release was in developing mice several-fold greater than the evoked GABA release, decreasing in magnitude with age. The potassium-stimulated release was only partially calcium dependent, more so with GABA in the adults and with taurine in the neonates, but a high magnesium ion concentration inhibited the release of both amino acids more strongly in the latter age group. Verapamil (0.1 mM) almost abolished the potassium stimulation of GABA release in both adult and neonate mice and was more effective on taurine release in neonate mice. The results suggest that taurine, not GABA, is the major inhibitor of excitability in developing mouse brain.