2022-04-282022-04-282004-08Büyükuysal, R. L. (2004). “Ischemia and reoxygenation induced amino acid release release and tissue damage in the slices of rat corpus striatum”. Amino Acids, 27(1), 57-67.0939-4451https://doi.org/10.1007/s00726-004-0073-9https://link.springer.com/article/10.1007/s00726-004-0073-9http://hdl.handle.net/11452/26234Ischemic incubation significantly increased amino acid release from rat striatal slices. Reoxygenation (REO) of the ischemic slices, however, enhanced only taurine and citrulline levels in the medium. Ischemia-induced increases in glutamate, taurine and GABA outputs were accompanied with a similar amount of decline in their tissue levels. Tissue final aspartic acid level, however, was doubled by ischemia. Lactate dehydrogenase (LDH) leakage was not altered by ischemia, but enhanced during REO. Presence of tetrodotoxine (TTX) during ischemic period caused significant decline in ischemia-induced glutamate output, but not altered REO-induced LDH leakage. Although omission of extracellular calcium ions from the medium during ischemic period protected the slices against REO-induced LDH leakage, this treatment failed to alter ischemia-induced glutamate and GABA outputs. The release of other amino acids, however, declined 50% in calcium-free medium. Blockade of the glutamate uptake transporter by L-trans-PDC, on the other hand, doubled ischemia induced glutamate and aspartic acid outputs. These results indicate that more than one mechanisms probably support the ischemia-evoked accumulation of glutamate and other amino acids in the extracellular space. Although LDH leakage enhanced during REO, processes involved in this increment were found to be dependent on extracellular calcium ions during ischemia but not REO period.eninfo:eu-repo/semantics/closedAccessBiochemistry and molecular biologyIschemiaReoxygenationGlutamate releaseAmino acidsLDHNitric-oxide synthaseOxygen-glucose deprivationInduced glutamate effluxIn-vitro ischemiaHippocampal slicesCerebral-cortexBrain-slicesCerebrocortical slicesAnoxic depolarizationNeuronal injuryAmino acidsAnimalsAnoxiaAspartic acidBrainCalciumCitrullineCorpus striatumFemaleGamma-aminobutyric acidGlutamic acidIonsIschemiaL-lactate dehydrogenaseMaleOxygenRatsRats, wistarReperfusion injuryTaurineTetrodotoxinTime factorsArticle0002232663000072-s2.0-4444279853576727115309572Biochemistry and molecular biologyDopamine; Catecholamines; 4-Hydroxyphenethylene GlycolAmino acid transportAnimal modelAnimal tissueArticleBrain ischemiaBrain tissueControlled studyCorpus striatumExtracellular calciumExtracellular spaceFemaleMaleNonhumanPriority journalRatReoxygenationTissue injury4 aminobutyric acidAmino acidAspartic acidCitrullineGlutamic acidLactate dehydrogenasePyrrolidine derivativeTaurineTetrodotoxin