Figure 7. Knockout of GluR2 in CA1 does not affect immediate early gene expression or seizure susceptibility.
(A) Confocal micrographs of cFOS-positive cells (green), detected by immunohistochemical staining, counterstained with nuclear marker DAPI (blue) in the CA1 of control and GluR2-cKO mice prior to training (‘no training’), following training (‘learning)’, and following kainate-induced seizures (KA) (n = 3 animals per group per genotype). Scale bar = 30 mm. (B) Quantitative analysis of cFOS-positive cells in the CA1 using stereology in control and GluR2-cKO mice that had no training or following training. Values shown as mean ± s.e.m. (C) Quantitative analysis of cFOS-positive cells in the CA1 using stereology in control and GluR2-cKO mice that had received a single i.p. injection of 25 mg/kg KA. Values shown as mean ± s.e.m. (D) Comparison of seizure susceptibility in control and GluR2-cKO animals. Seizure score is defined as the total seizure score divided by the number of observations and plotted as a cumulative frequency step graph – see experimental methods regarding seizure score scale. As the data were not normally distributed they were analyzed by Mann-Whitney. The Benjamini-Hochberg FDR correction was applied to correct for the multiple t-tests performed. No significant difference between curves was observed.
