Saransaari P, Oja S S
Tampere Brain Research Center, University of Tampere Medical School, Finland.
Neuroscience. 1999;94(3):949-54. doi: 10.1016/s0306-4522(99)00384-x.
Taurine release in the developing hippocampus is markedly potentiated in ischemia. The mechanisms of the ischemia-induced release were studied in hippocampal slices from seven-day-old mice using a superfusion system. The basal release of [3H]taurine was significantly increased in media under normal conditions, but the ischemia-evoked release decreased in Na+ -free media, indicating the participation of Na+ -dependent transport processes. The involvement of taurine transporters in the release was confirmed with the structural analogs, hypotaurine and beta-alanine. These amino acids potentiated the release by trans-stimulation, but not in Na+ -free media. In the absence of Ca2+, the basal taurine release was markedly increased in normoxia but diminished in ischemia, indicating that a part of basal taurine release in ischemia is Ca2+ dependent. On the other hand, the K+ stimulation of taurine release was preserved in Ca2+ -free medium. The phospholipase and protein kinase inhibitors had no effect on ischemia-induced taurine release, nor did the chloride channel blockers 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (2 mM) and diisothiocyanostilbene-2,2'-disulfonate (0.1 mM) affect the release in ischemia. The increase in extracellular levels of taurine in the immature hippocampus in ischemia may serve as an important protective mechanism against excitotoxicity, to which the developing brain is particularly vulnerable, and contribute to the resistance of the immature brain to hypoxia.
