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Excitotoxic activation of postsynaptic N-methyl-d-aspartate (NMDA) receptors is thought to be a key event for the molecular pathogenesis of postischemic delayed neuronal death in CA1 hippocampus. To assess a possible interference of ischemia with NMDA receptor expression, transcription of the NMDA receptor 1 (NMDA-R1) gene was examined by in situ hybridization in the gerbil brain after 5 min of global ischemia and various recirculation intervals. In normal gerbil brain, NMDA-R1 was strongly expressed and equally abundant in CA1 and CA3 neurons. After ischemia, expression remained unchanged for 24 h, followed by a selective decline in mRNA levels in CA1 neurons, resulting in the complete disappearance of hybridization signals after 4 days. NMDA-R1 expression in forebrain neurons less vulnerable or resistant to ischemia including CA3 and dentate granule cells remained unchanged. Similar in situ data were obtained for the β subunit of the inhibitory glycine receptor (Gly-R). This subunit is also abundantly expressed in the pyramidal cell layer of the hippocampus, but not known to be involved in the mechanisms of postischemic excitotoxicity.

NMDA and Glycine Receptor mRNA Expression following Transient Global Ischemia in the Gerbil Brain