In vitro hypoxia induces expression of the NR2C subunit of the NMDA receptor in rat cortex and hippocampus.

In mammalian brain, ischemic injury could be mediated by delayed glutamate neurotoxicity. We have studied the possibility of altered genetic expression of quiescent NMDA receptor subunits in an in vitro model of hypoxia-hypoglycemia, using the reverse transcription-polymerase chain reaction technique. It was found that mRNA corresponding to the NR2C subunit was present 1 h after a brief hypoxic-hypoglycemic episode in adult rat hippocampus and cortex but absent in control tissue. These findings indicate that the phenotypic characteristics of certain brain cells after an ischemic insult are altered by the expression of genes that are quiescent in those cells under normal physiological conditions.