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Changes in hippocampal NMDA‐R subunit composition induced by exposure of neonatal rats to l ‐glutamate
Author(s) -
RiveraCervantes M.C.,
FloresSoto M.E.,
ChaparroHuerta V.,
ReyesGómez J.,
FeriaVelasco A.,
Schliebs R.,
BeasZárate C.
Publication year - 2009
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2008.09.006
Subject(s) - glutamate receptor , nmda receptor , excitotoxicity , hippocampal formation , protein subunit , biology , hippocampus , endocrinology , messenger rna , medicine , cerebral cortex , neuroscience , receptor , biochemistry , gene
Overactivation of NMDA‐Rs may mediate excitotoxic cell death associated with epileptic seizures, and hypoxic–ischemic conditions. We assessed whether repeated subcutaneous administration of l‐ glutamate to neonatal rats affects the subunit composition of NMDA‐Rs. Accordingly, cortical and hippocampal tissue from 14‐day‐old rats was analyzed by Western blotting and RT‐PCR to quantify the protein and mRNA expression of different NMDA‐R subunits. In addition, tissue sections were Nissl stained to assess the cell damage in this tissue. Early exposure of neonatal rats to l‐ glutamate differentially affects the expression of mRNA transcripts for NMDA‐R subunits in the cerebral cortex and hippocampus. In the cerebral cortex, a decrease in NR2B subunit mRNA expression was observed, as well as a loss of NR1 and NR2A protein. By contrast, neonatal l‐ glutamate administration augmented the transcripts encoding the NR1, NR2B, and NR2C subunits in the hippocampal formation. The expression of mRNA encoding the NR2A subunit was not affected by neonatal l‐ glutamate administration in either of the brain regions examined. This differential expression of NMDA‐R subunits following neonatal exposure to l‐ glutamate may represent an adaptive response of the glutamate receptors to overactivation in order to reduce the effect of high l‐ glutamate during the early period of life when the animal is more vulnerable to excitotoxicity.