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   <subfield code="a">Amino-acid release from human cerebral cortex during simulated ischaemia in vitro</subfield>
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   <subfield code="c">[E. Hegstad, J. Berg-Johnsen, T. Haugstad, E. Hauglie-Hanssen, I. Langmoen]</subfield>
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   <subfield code="a">Summary: The aim of the present study was to investigate the release of amino-acids in human cerebral cortex during membrane depolarization and simulated ischaemia (energy deprivation). Superfluous tissue from temporal lobe resections for epilepsy was cut into 500 μm thick slices and incubated in vitro. Membrane depolarization with 50 mM K+ caused a release of glutamate, aspartate, GABA and glycine, but not glutamine or leucine. The release of glutamate and GABA was Ca++-dependent. Slices were exposed to simulated ischaemia (energy deprivation; ED) by combined glucose/oxygen deprivation. This caused a Ca++-indepedent release of glutamate, aspartate, GABA, glycine, and taurine which started after 8 min, peaked at the end or shortly after the 27 min period of ED, and returned to control levels within 11 min following termination of ED. Preloaded D-[3H]aspartate was released both during K+-stimulation and ED. Release of D-[3H]aspartate during ED was delayed compared to glutamate supporting an initial phase of synaptic glutamate release. Uptake of L-[3H]glutamate was increased during the period of glutamate release, suggesting passive diffusion across the cell membrane or enhanced transport efficacy in cellular elements with functioning uptake mechanisms.</subfield>
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   <subfield code="u">Institute for Surgical Research and Department of Neurosurgery, Rikshospitalet, The National Hospital, University of Oslo, Norway</subfield>
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