Properties of spontaneous and evoked release of taurine from hypothalamic crude P2 synaptosomal preparations

Recent studies suggest that taurine may function as a neurotransmitter in the hypothalamus. We examined this role for taurine by characterizing the high K+- and veratridine-evoked release, and the spontaneous release of [3H]taurine from superfused synaptosomal pellets (once-washed crude P2 fractions) prepared from rat hypothalami. Exposure of washed crude P2 synaptosomal pellets which had been preloaded with a concentration of [3H]taurine (1.5 microM) in the high affinity uptake range to either 56 mM K+ or 100 microM veratridine evoked a Ca2+-independent release of [3H]taurine. Exposure of washed crude P2 synaptosomal pellets, which had been preloaded with a concentration of [3H]taurine (2 mM) in the low affinity uptake range to 56 mM K+, induced a Ca2+-independent release of [3H]taurine, whereas 100 microM veratridine did not, either in the presence or absence of Ca2+. These observations support the hypothesis that the high affinity uptake system is located on neuronal membranes with evoked release occurring from a non-vesicular pool of taurine in the neuronal cytoplasm. In contrast, the low affinity uptake system appears to be located on glial membranes with evoked release occurring from a pool of taurine in the glial cytoplasm. Spontaneous [3H]taurine efflux from the high affinity uptake pool in the crude P2 synaptosomal pellet was not Ca2+-dependent. Furthermore, efflux was significantly reduced when NaCl was osmotically replaced with choline chloride in the superfusing medium. These observations suggest that the evoked release of taurine is not simply a reversal of the Na+-dependent high affinity taurine uptake carrier, but accomplished through some other unknown mechanism. The results presented in this report do not support a neurotransmitter role for taurine in the hypothalamus.