Skip to main content
Figure 6 | BMC Neuroscience

Figure 6

From: GT1b-induced neurotoxicity is mediated by the Akt/GSK-3/tau signaling pathway but not caspase-3 in mesencephalic dopaminergic neurons

Figure 6

Phosphorylation of tau is increased by GT1b treatment in mesencephalic cultures. Double-immunostaining with AT8 (Ser202; green)) for phospho-tau and TH (red) for DA neurons in mesencephalic cultures treated with vehicle (A) or 20 μg/ml GT1b (B) for 8 h. (D-I) Double-immunostaining showed Tau hyperphosphorylation in the GT1b-injected SN. SN tissues were prepared 72 h after PBS (D-F) or GT1b (60 μg/3 μl, G-I) injection, processed for immunostaining with TH antibody alone (C), double-immunostaining with AT8 (D, G, green) and TH (E, H, red) antibody, and then both images were merged (F, I). Scale bar, 10 μm in A-C, 200 μm in F and 50 μm G-I. SNpc, substantia nigra pars compacta; SNr, substantia nigra reticulata; VTA, ventral tegmental area. (J,K) Cell lysates were analyzed by Western blot analysis with AT8 (Ser202) antibody at indicated time points. After membrane stripping, blots were then reprobed with actin antibody. The histogram shows quantitation of tau phosphorylation. (L.M) Tau phosphorylation is reversed by L803-mt, GSK-3 inhibitor in GT1b-treated mesencephalic cultures. The histogram shows quantitation of tau phosphorylation. The values represent the mean ± SEM of triplicate cultures in three to five separate samples. *P < 0.001, **P < 0.01 significant from non-treated cultures; #P < 0.01, significant from GT1b-treated cultures (ANOVA and Student-Newman-Keuls analyses). C, control; G, GT1b; L, L803mt.

Back to article page