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Fig. 4 | Molecular Brain

Fig. 4

From: A new mouse line with reduced GluA2 Q/R site RNA editing exhibits loss of dendritic spines, hippocampal CA1-neuron loss, learning and memory impairments and NMDA receptor-independent seizure vulnerability

Fig. 4

Altered Hippocampal dendritic morphology and neural populations. a NeuN+ cells in the hippocampus (10x magnification) and CA1 region (100x magnification) of WT and GluA2+/ECS(G) mice. b Cell loss was suggested in the CA1 but not CA3 region of the hippocampus in young adult GluA2+/ECS(G) mice as compared to WT littermates (n=5 mice/genotype; unpaired t-test). c GFAP+ cell quantification in the CA1 and CA3 of GluA2+/ECS(G) mice as compared to WT littermates (n=3 mice/genotype). d IBA1+ cell quantification in the CA1 and CA3 of GluA2+/ECS(G) mice as compared to WT littermates (n=3 mice/genotype). e Inset: Representative traces of CA1 hippocampal neurons from GluA2+/ECS(G) and WT littermates. GluA2+/ECS(G) mice exhibit decreases in dendritic intersections compared to WT controls (n=3 neurons/brain, 3 brains/genotype (total 9 neurons/genotype) (two-way ANOVA, * = significant main effect of genotype on distance from soma). f Inset: Representative images of CA1 apical dendritic spines from GluA2+/ECS(G) and WT littermates. GluA2+/ECS(G) mice have significantly less spines compared to WT littermates (n= 3 dendrites/neuron, 3 neurons/brain, 3 (WT) and 2 (GluA2+/ECS(G)) brains/genotype (total 27 (WT) and 18 (GluA2+/ECS(G)) apical dendrites/genotype); unpaired t-test). All experiments in Fig. 4 were conducted in 8–10-week-old mice. Data in (b), (c), (d) and (f) represent mean ± SD and in (e) represent mean ± SEM

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