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. 2018 Apr 6;11:100. doi: 10.3389/fnmol.2018.00100

Figure 6.

Figure 6

SNC80 treatment reduces oxidative stress in interneurons from stratum radiatum of CA1 HPC. In (A–C), representative pictures of neurons (N) in the radiatum layer (Rad) of CA1 region in ventral HPC after RSD without treatment (NT), in control, resilient and vulnerable mice, are shown respectively. In (D–F), pictures of neurons from the Rad layer of CA1 in vHPC after RSD with SNC80 treatment (SNC80), in control, resilient and vulnerable mice, respectively. Scale bar = 500 nm. In (G–J), magnified views of dilated ER, dilated Golgi apparatus (go), lipofuscin granule (li), and nuclear indentation (id), respectively. In (K–O), graphs for Rad layer representing the proportion of dark neurons, the proportion of neurons presenting dilated ER, dilated Golgi apparatus, lipofuscin granules and indentations, respectively, without and with SNC80 treatment. Two-way ANOVA, Bonferroni post hoc analysis, N(NT: C; R; V) = 23; 24; 26 cells, and N(SNC80: C; R; V) = 25; 24; 26 cells. The two analyzed factors are the stress phenotype (blue, green and red bars for control, resilient and vulnerable mice under RSD, respectively) and the presence or absence of SNC80 treatment (dark blue, green and red bars for control, resilient and vulnerable mice under RSD without SNC80 treatment, respectively, and pale blue, green and red bars with a streaky pattern for control, resilient and vulnerable mice under RSD with SNC80 treatment, respectively). Significance: * for stress phenotype effect or #for SNC80 treatment effect or for stress × treatment effect, ∧(Control vs. Vulnerable), &(Control vs. Resilient), +(Resilient vs. Vulnerable) = ++p < 0.01, ###,∧∧∧p < 0.001, ####, &&&&p < 0.0001. Error bars are mean ± SEM.