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. Author manuscript; available in PMC: 2010 Oct 6.
Published in final edited form as: Cell Death Differ. 2009 Sep 25;17(3):459–468. doi: 10.1038/cdd.2009.134

Figure 4. Genotype and phenotype analysis of bim−/− mice.

Figure 4

(A) Representative PCR showing genotyping of mice. (B) Representative Western blot (n = 2 per lane) confirming normal expression of KA receptor GluR6/7 in the mouse amygdala between wild-type (wt) and bim knockout mice. Actin is shown as a control for protein loading. (C) Representative Western blots of hippocampal samples confirming Bim deficiency in bim−/− mice, while levels of a selection of other proteins are normal. (D) Representative photomicrographs of NeuN-stained CA3 subfields from wild-type and bim−/− mice. (E) Graphs showing counts of NeuN-positive cells in various hippocampal fields. No differences were evident between mice of the two genotypes (n = 3 per group). (F) Graphs showing EEG data on seizure parameters between wild-type and bim−/− mice following intra-amygdala KA microinjection. No differences were found between mice of the two genotypes (n = 9–10 per group).

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