Abstract
During brain ischaemia there is a sustained increase in extracellular glycine levels, and the potential role of these changes in modulating N-methyl- d-aspartate (NMDA) receptor-mediated activity following an anoxic/aglycaemic insult was studied in the rat hippocampal slice. Addition of large saturating concentrations of glycine (100 μM and 1 mM) to the superfusate resulted in increased extracellularly recorded NMDA receptor-mediated components of excitatory postsynaptic potentials (EPSPs) recorded in area CA1. The effects of added glycine were strychnine-insensitive and blocked by a competitive NMDA antagonist. Anoxic/aglycaemic insults to the tissue caused persistent increases in NMDA receptor-mediated EPSPs, but the magnitude of the observev upregulation was uaffected by the presence of added saturating concentrations of glycine. The data suggests that alterations in glycine levels after oxygen deprivation are not responsible for the long term modulation of NMDA receptor activity.
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