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. 2018 Sep 18;19(9):2811. doi: 10.3390/ijms19092811

Figure 1.

Figure 1

Treatment with SA4503 reverses abnormality of axonal development and dendritic filopodia in cultured AtrxΔE2 (Atrx mutant mice lacking exon 2) neurons. (A) Representative images of EGFP-transfected cortical neurons at DIV5. Neurons are stained for anti-GFP. Images in the middle and bottom panels are enlarged from the corresponding boxed areas. Scale bars: top panels, 50 µm; middle panels, 10 µm; bottom panels, 5 µm. (B) Total axonal length. ** p < 0.01, versus vehicle-treated WT (wild type) neurons; ## p < 0.01, versus vehicle-treated AtrxΔE2 neurons by one-way ANOVA with post-hoc Tukey’s test; F (3, 76) = 17.4; n = 20 neurons for each group. The experiments were repeated three times with similar results. (C) Data show the number of filopodia per 20 µm dendritic length. ** p < 0.01, versus vehicle-treated WT neurons; ## p < 0.01, versus vehicle-treated AtrxΔE2 neurons by one-way ANOVA with post hoc Tukey’s test; F (3, 76) = 48.26; n = 20 neurons for each group. The experiments were repeated three times with similar results. Each bar represents the mean ± SEM. Abbreviations: Veh., vehicle; SA, SA4503.