Systemic administration of
kainic acid in C57BL/6 and FVB/N mice induces a comparable level of seizure induction yet results in differential susceptibility to seizure-induced cell death. While
kainate administration causes severe hippocampal damage in mice of the FVB/N strain, C57BL/6 mice display no demonstrable cell loss or damage. At present, while the cellular mechanisms underlying strain-dependent differences in susceptibility remain unclear, some of this variation is assumed to have a genetic basis. As
glutamate receptors are thought to participate in seizure induction and the subsequent neuronal degeneration that ensues, previous studies have proposed that variation in the precise subunit composition of
glutamate receptors may result in differential susceptibility to excitotoxic cell death. Thus, we chose to examine the relationship between the cellular distribution and expression of
glutamate receptor subunit
proteins and cell loss within the hippocampus in mouse strains resistant and susceptible to
kainate-induced excitotoxicity. Using semi-quantitative Western blot techniques and immunohistochemistry with the use of
antibodies that recognize subunits of the KA (GluR5,6,7),
AMPA (GluR1, GluR2, and GluR4), and
NMDA (
NMDAR1 and NMDAR2A/2B) receptors, we found no significant strain-dependent differences in the expression or distribution of these
glutamate receptor subunits in the intact hippocampus. Following
kainate administration, expression changes in
ionotropic glutamate receptor subunits paralleled the development of susceptibility to cell death in the FVB/N strain only. Strain differences in hippocampal vulnerability to
kainate-induced
status epilepticus are not due to
glutamate receptor protein expression.