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

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Abstract
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.