Taurine release modified by nitric oxide-generating compounds in the developing and adult mouse hippocampus.

The effects of the nitric oxide-generating compounds hydroxylamine, sodium nitroprusside and S-nitroso-N-acetylpenicillamine, and the nitric oxide synthase inhibitors nitroarginine and 7-nitroindazole on taurine release from hippocampal slices from adult (three-month-old) and developing (seven-day-old) mice were characterized using a superfusion system. The basal release of [3H]taurine was enhanced when the nitric oxide donors were added at the beginning of superfusion, more markedly in the adult than in the immature hippocampus. The effect of hydroxylamine was clearly concentration-dependent. Hydroxylamine also markedly enhanced the release of endogenous taurine. The K+-stimulated (50 mM) release of taurine was generally inhibited by the nitric oxide-generating compounds in both age groups. Nitric oxide is thus able to act directly at presynaptic terminals, modulating taurine release as a retrograde messenger. The N-methyl-D-aspartate-evoked taurine release was reduced by the nitric oxide donors, particularly by sodium nitroprusside, in the adult hippocampus, while hydroxylamine and S-nitroso-N-acetylpenicillamine markedly potentiated the release in developing mice. In the immature hippocampus the hydroxylamine-enhanced taurine release seems to involve a Ca2+-independent, Na+-dependent and carrier-mediated process while in adult mice only a part of the hydroxylamine-enhanced release is mediated by the same mechanism. The results show that nitric oxide-generating compounds modify the basal, K+- and N-methyl-D-aspartate-evoked releases of taurine in both adult and immature hippocampus. The enhanced N-methyl-D-aspartate receptor-evoked release may be an important mechanism protecting the immature brain against excitotoxicity.