Superfusion of synaptosomes prepared from rat olfactory bulb revealed
constant basal release of endogenous taurine (Tau), aspartate (Asp), g
lutamate (Glu) and gamma-aminobutyrate (GABA): their release rates wer
e 110.4 +/- 13.0, 30.3 +/- 6.7, 93.7 +/- 13.1, and 53.3 +/- 8.8 pmol/m
in/mg protein, respectively. The depolarizing-stimulation with 30mM KC
l evoked 1.17-, 2.18-, 2.55- and 1.53-fold increases, respectively. Ta
u release was calcium-independent. However, the perfusion of synaptoso
mes with Tau (10 mu M) inhibited the evoked increase in GABA release b
y 63% without changing basal release, although it did not affect relea
se of Asp and Glu. Phaclofen (10 mu M, a GABA, receptor antagonist), b
ut not bicuculline (10 mu M, a GABA, receptor antagonist), counteracte
d the Tau-induced reduction in GABA release. These data suggest that T
au may be abundantly released from nerve endings of rat olfactory bulb
and that it may regulate GABA release through the activation of presy
naptic GABA(B) autoreceptors.