Modulation of taurine release in ischemia by glutamate receptors in mouse brain stem slices.
Glutamate is the main excitatory transmitter in the brain stem, regulating many vital sensory and visceral processes. Taurine is inhibitory and functions as a neuromodulator and regulator of cell volumes in the brain, being especially important in the developing brain. Taurine release is markedly enhanced under ischemic conditions in many brain areas, providing protection against excitotoxicity. The involvement of glutamate receptors in the release of preloaded [(3)H]taurine was now characterized under ischemic conditions in slices prepared from the mouse brain stem from developing (7-day-old) and young adult (3-month-old) mice. The ionotropic glutamate receptor agonists N-methyl-D-aspartate, kainate, and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate had no effect on ischemic taurine release in the immature brain stem, whereas in adults the release was enhanced in a receptor-mediated manner. The metabotropic receptor agonists of group I, (1+/-)-1-aminocyclopentane-trans-1,3-dicarboxylate and (S)-3,5-dihydroxyphenylglycine, potentiated both basal and K(+)-stimulated release in both age groups. The group III agonist L(+)-2-amino-4-phosphonobutyrate also enhanced the release. In both cases the effects were receptor-mediated, being reduced by the respective antagonists. The results show that activation of glutamate receptors in the ischemic brain stem generally enhances the release of taurine. This is beneficial to neurons in ischemia, offering protection against excitotoxicity and preventing neuronal damage.
PubMed Abstracts
PubMed Abstracts