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Journal of Neuroscience, Vol 14, 2697-2707, Copyright © 1994 by Society for Neuroscience
Kainate-induced status epilepticus alters glutamate and GABAA receptor gene expression in adult rat hippocampus: an in situ hybridization study
LK Friedman, DE Pellegrini-Giampietro, EF Sperber, MV Bennett, SL Moshe and RS Zukin
Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461.
In adult rats, intraperitoneal administration of kainic acid, a glutamic
acid analog and potent neurotoxin, induces persistent seizure activity that
results in electrographic alterations and neuropathology that closely
resemble human temporal lobe epilepsy. We used in situ hybridization to
identify regions of altered glutamate and GABAA receptor gene expression
following kainate-induced status epilepticus. In the CA3/CA4 area, the
hippocampal region most vulnerable to neurodegeneration after kainate acid
treatment, expression of GluR2 (the AMPA/kainate receptor subunit that
limits Ca2+ permeability) and GluR3 was decreased markedly at 12 and 24 hr,
times preceding neurodegeneration. These findings raise the possibility
that increased formation of Ca(2+)-permeable AMPA/kainate receptors in the
CA3/CA4 area may enhance glutamate pathogenicity. Expression of the GABAA
alpha 1, subunit was also reduced, indicating a possible decrease in
inhibitory transmission, which would also enhance excitotoxicity. GluR1 and
NR1 expression was not significantly changed. In the dentate gyrus, a
region resistant to neurodegeneration, concomitant increases in GluR2 and
GluR3 expression were observed; GluR1, NR1, and GABAA alpha 1 mRNAs were
not detectably altered. Analysis of emulsion-dipped sections revealed that
the changes in GluR2, GluR3, and GABAA alpha 1 expression represented
changes in mRNA content per neuron and were specific to pyramidal cells of
the CA3/CA4 area and to granule cells of the dentate gyrus. These findings
indicate that kainate seizures modify hippocampal glutamate and GABAA
receptor expression in a cell-specific manner. Timing of the changes in
glutamate and GABAA receptor mRNAs indicates that these changes may play a
causal role in hippocampal neuronal cell loss following kainate-induced
seizures.
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