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In Vitro Hypoxia Induces Expression of the NR2C Subunit of the NMDA Receptor in Rat Cortex and Hippocampus
Author(s) -
PerezVelazquez Jose L.,
Zhang Liang
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.63031171.x
Subject(s) - nmda receptor , glutamate receptor , hypoxia (environmental) , protein subunit , hippocampus , biology , cerebral cortex , in vitro , messenger rna , cortex (anatomy) , receptor , neuroscience , microbiology and biotechnology , endocrinology , chemistry , medicine , gene , biochemistry , organic chemistry , oxygen
Abstract: 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.