For the purpose of demonstrating the action of taurine as a neuromodulator in addition to its suggested neurotransmitter function, the effects of taurine and muscimol on the depolarization-induced Ca-dependent release of [3H] gamma-aminobutyric acid ([3H]GABA) and L-[3H]glutamate in cerebellar slices from guinea pigs were investigated. The release of [3H]GABA was found to be greatly decreased by a GABA agonist, muscimol, and by taurine, but not by glycine. The release of L-[3H]glutamate was little affected by taurine. The release of [3H]GABA, was enhanced by bicuculline and strychnine, but not by picrotoxin, and the suppressive action of muscimol on the GABA release was antagonized by bicuculline, picrotoxin, and strychnine, suggesting the possible existence of presynaptic autoreceptors for GABA in the cerebellum. The suppressive action of taurine on the release of [3H]GABA, on the other hand, was blocked only by bicuculline. These results suggest that taurine reduced the release of [3H]GABA from cerebellar slices by acting on the GABA autoreceptors or, more likely, on other types of receptors that are sensitive to bicuculline. As a possible mechanism for this modulatory action of taurine, the blockade by this amino acid of the influx of Ca2+ into cerebellar tissues was tentatively suggested.

Abstract— GABA, taurine and β‐alanine are taken up by guinea‐pig cerebellar slices by both the high‐and low‐affinity uptake processes, whereas glycine is taken up only by the low‐affinity process. A considerable amount of labelled GABA loaded in the slice is released by unlabelled external GABA and a minute amount is released by external β‐alanine, glycine and taurine. External glycine and β‐alanine releases labelled glycine loaded in the slice. Labelled taurine loaded is effectively released by external taurine and β‐alanine, while labelled β‐alanine loaded is released only by external β‐alanine. It is suggested that hetero‐exchanges which are one‐directional in some cases also take place between the amino acids in addition to homo‐exchanges. Therefore, high‐affinity uptake processes observed with GABA and taurine could be the result of the homo‐exchange diffusions, while that of β‐alanine could be due to either the homo‐exchange or the hetero‐exchange diffusions or both. K+′‐evoked releases of GABA and to a lesser extent, taurine are partially dependent upon the presence of Ca+ in the superfusion media, whereas that of glycine and probably that of β‐alanine, are not, K+ ‐evoked releases of labelled GABA and taurine are larger when loaded by their high‐affinity uptake systems than by their low‐affinity uptake processes. The reverse is the case with labelled glycine and β‐alanine. These results do not rule out the possibility that taurine might act as a neurotransmitter in the cerebellum.

No abstract

No abstract

No abstract