title: Extracellular taurine as a parameter to monitor cerebral insults 'on-line': time courses and mechanisms as studied in vivo.
abstract: Taurine increases in the zone surrounding a thrombotic infarct which could be prevented by a neuroprotective drug. Therefore, we aimed at studying the possible release mechanisms since the monitoring of taurine might give valuable information on the progress of cerebral insults and the effect of drugs. A microdialysis membrane was implanted into the cortex of anaesthetised rats: As toxic triggers possibly released by the dying cells in the peri-infarct zone, either a glutamatergic agonist (NMDA) or high potassium were applied via the microdialysis probe. Alternatively, a diluted perfusate was applied to induce cell swelling directly. NMDA antagonists or the NO synthase inhibitor L-NAME were applied locally too. NMDA, NO, high potassium or the hypotonic solution stimulated the release of taurine. The effect of high potassium could be prevented by Ketamine, but not by APV. The effect of NMDA could be inhibited by APV or Ketamine or the NO synthase inhibitor L-NAME. The release of taurine induced by the hypotonic solution could not be be reduced by any of the inhibitors. These data suggest that the release of taurine induced by glutamatergic activity is mediated via the NO cascade. The potassium mediated release seems to be related only in part to glutamatergic activity. Thus, other mechanisms seem to be predominate in potassium mediated swelling. Hypoosmotically induced taurine release is not mediated via the NO cascade and also seems to differ from the aforementioned release mechanisms.
  
  
  CONCLUSIONS
  Monitoring of extracellular taurine allows to follow pathological events and to differentiate drug effects.
authors.affiliation: Janssen-Cilag GmbH, Drug Discovery, Neuss, Germany.
authors.forename: D K
authors.initials: DK
authors.lastname: Scheller
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space; D018698:Glutamic Acid / Q000378:metabolism*; D007038:Hypotonic Solutions / Q000494:pharmacology; D008297:Male; D016202:N-Methylaspartate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013654:Taurine / Q000378:metabolism*; D013997:Time Factors; D014882:Water-Electrolyte Balance / Q000502:physiology*
chemical_list: D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D007038:Hypotonic Solutions; D013654:Taurine; D018698:Glutamic Acid; D016202:N-Methylaspartate; D011188:Potassium