title: Taurine release in mouse brain stem slices under cell-damaging conditions.
abstract: Taurine has been thought to be essential for the development and survival of neural cells and to protect them under cell-damaging conditions. In the brain stem taurine regulates many vital functions, including cardiovascular control and arterial blood pressure. We have recently characterized the release of taurine in the adult and developing brain stem under normal conditions. Now we studied the properties of preloaded [3H]taurine release under various cell-damaging conditions (hypoxia, hypoglycemia, ischemia, the presence of metabolic poisons and free radicals) in slices prepared from the mouse brain stem from developing (7-day-old) and young adult (3-month-old) mice, using a superfusion system. Taurine release was greatly enhanced under these cell-damaging conditions, the only exception being the presence of free radicals in both age groups. The ischemia-induced release was characterized to consist of both Ca2+-dependent and -independent components. Moreover, the release was mediated by Na+-, Cl--dependent transporters operating outwards, particularly in the immature brain stem. Cl- channel antagonists reduced the release at both ages, indicating that a part of the release occurs through ion channels, and protein kinase C appeared to be involved. The release was also modulated by cyclic GMP second messenger systems, since inhibitors of soluble guanylyl cyclase and phosphodiesterases suppressed ischemic taurine release. The inhibition of phospholipases also reduced taurine release at both ages. This ischemia-induced taurine release could constitute an important mechanism against excitotoxicity, protecting the brain stem under cell-damaging conditions.
authors.affiliation: Tampere Brain Research Center, Medical School, University of Tampere, and Centre for Laboratory Medicine, Tampere University Hospital, Finland. blpisa@uta.fi
authors.forename: P
authors.initials: P
authors.lastname: Saransaari
authors.forename: S S
authors.initials: SS
authors.lastname: Oja
mesh_terms: D019297:2,4-Dinitrophenol / Q000633:toxicity*; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D001933:Brain Stem / Q000254:growth & development / Q000378:metabolism* / Q000473:pathology; D020013:Calcium Signaling / Q000187:drug effects; D006152:Cyclic GMP / Q000378:metabolism; D005260:Female; D006162:Guanylate Cyclase; D006861:Hydrogen Peroxide / Q000633:toxicity*; D007003:Hypoglycemia / Q000378:metabolism*; D007473:Ion Channels / Q000378:metabolism; D008297:Male; D051379:Mice; D008867:Microtomy; D018696:Neuroprotective Agents / Q000378:metabolism*; D016877:Oxidants / Q000633:toxicity*; D011493:Protein Kinase C / Q000378:metabolism; D049992:Sodium Chloride Symporters / Q000378:metabolism; D013654:Taurine / Q000378:metabolism*; D014475:Uncoupling Agents / Q000633:toxicity*
chemical_list: D007473:Ion Channels; D018696:Neuroprotective Agents; D016877:Oxidants; D049992:Sodium Chloride Symporters; D014475:Uncoupling Agents; D013654:Taurine; D006861:Hydrogen Peroxide; D011493:Protein Kinase C; D006162:Guanylate Cyclase; D006152:Cyclic GMP; D019297:2,4-Dinitrophenol