Abstract In brain slices the mechanisms of release of GABA have been extensively studied, but those of taurine markedly less. The knowledge acquired from studies on GABA is, nevertheless, still fragmentary, not to speak of that obtained from the few studies on taurine, and firm conclusions are difficult, even impossible, to draw. This is mainly due to methodological matters, such as the diversity and pitfalls of the techniques applied. Brain slices are relatively easy to prepare and they represent a preparation that may most closely reflect relations prevailing in vivo, since the tissue structure and cellular integrity are largely preserved. In our opinion the most recommendable method at present is to superfuse freely floating agitated slices in continuously oxygenated medium. Taurine is metabolically rather inert in the brain, whereas the metabolism of GABA must be taken into account in all release studies. The use of inhibitors of GABA catabolism is discouraged, however, since a block in GABA metabolism may distort relations between different releasable pools of GABA in tissue. It is not known for sure how well, and homogeneously, incubation of slices with radioactive taurine labels the releasable pools but at least in the case of GABA there may prevail differences in the behavior of labeled and endogenous GABA. It is suggested therefore that the results obtained with radioactive GABA or taurine should be frequently checked and confirmed by analyzing the release of respective endogenous compounds. The spontaneous efflux of both GABA and taurine from brain slices is very slow. The magnitude of stimulation of GABA release by homoexchange is greater than that of taurine under the same experimental conditions. However, the release of both amino acids is generally enhanced by a great number of structural analogs, the most potent being those which are simultaneously the most potent inhibitors of uptake. This may result in part from inhibition of reuptake of amino acid molecules released from slices but the findings may also signify that the efflux of GABA and taurine is at least partially mediated by the membrane carriers operating in an outward direction. It is thus advisable not to interpret that stimulation of release in the presence of uptake inhibitors solely results from the block of reuptake of exocytotically release molecules, since changes in the carrier-mediated transport are also likely to occur upon stimulation. The electrical and K + stimulation evoke the release of both GABA and taurine. The evoked release of GABA is several-fold greater than that of taurine in slices from the adult brain. During ontogeny, the K +-stimulated release of GABA is initially very low, increasing strikingly towards adulthood. In contrast, the response of taurine release to K + is slow but strikingly large in the immature brain, decreasing gradually during development. In fact, the evoked release of taurine has been in the developing brain several-fold greater than the evoked release of GABA in every brain area studied. This relationship is drastically altered with advancing age. These results emphasize the importance of taurine in regulation of excitability in the immature brain. No marked changes occur in the basal or evoked release of GABA and taurine in different brain areas during ageing. A salient feature of the stimulated release of taurine is a slow and prolonged time course, while the responses in the release of GABA are prompt. The K +-dependence curves are similar for GABA and taurine, however. An omission of Na + ions causes a more pronounced release of taurine than that of GABA from slices. The membrane Na + channels and Na +/K +-ATPases are apparently involved in the regulation of the release. In most brain regions the major part of the K +-stimulated release of GABA has been dependent on Ca 2+, whereas the electrically or veratridine-evoked release has shown less Ca 2+ dependency. The Ca 2+-independent release may occur concomitantly with the Ca 2+-dependent release and take place via the high-affinity transport sites of GABA. The stimulated release of GABA is generally more Ca 2+ dependent in the adult than developing brain. The stimulated release of taurine is likewise Ca 2+ dependent, the dependency being greater in the immature than mature brain. The evaluation as to whether or not the K +-stimulated release is dependent on Ca 2+ is hampered by the great enhancement of basal release in Ca 2+-free media, more so in the case of taurine than GABA. Excitatory amino acids and their agonists evoke release of GABA and taurine from brain slices. The stimulated release of taurine from cerebral cortical slices is massively greater in developing than in adult mice. Furthermore, the NMDA and AMPA (quisqualate) subtypes of glutamate receptors could be involved in the stimulation of taurine release in low-K + media, whereas both NMDA- and kainate-sensitive receptors may regulate the K +-stimulated release. Effects of drugs have been tested almost exclusively on the release of GABA. The drugs that interact with Na + movements across plasma membranes affect the release of GABA as well. Other effective drugs include barbiturates, convulsant alkaloids, anticonvulsants, tetanus toxin, diazepam, haloperidol and imipramil, to mention only those that have been reliably shown to exert an influence. No drugs that affect specifically only the release of GABA or taurine are known at present. Taurine has been demonstrated to interfere with both GABA A and GABA B receptors. This may be the reason why taurine is able to modulate the K +-stimulated release of GABA. On the other hand, GABAergic substances modify the release of taurine from brain slices. The importance of dopamine as a modulator of the release of GABA has been extensively studied, though the results are largely contradictory. The excitatory and inhibitory effects of dopamine on the release of GABA may be explained by the actions of the different subtypes of dopamine receptors. The release of taurine from striatal slices is also modified by presynaptic dopamine receptors. It has been suggested recently that the release of taurine solely results from cell volume regulation and water movements across plasma membranes. These ideas mainly stem from data obtained in experiments carried out with cultured astrocytes and cerebellar granule cells. In brain slices the matter is not so simple, since intracellular swelling in slices cannot be the only factor responsible for the enhanced release of taurine under the influence of depolarizing agents. The general properties of the evoked release of taurine show, however, that a major part of it must be due to processes other than exocytosis of synaptic vesicles.