Skip to main content
Figure 5 | BMC Neuroscience

Figure 5

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

Figure 5

GT1b increases the activity GSK-3β by dephosphorylation in neuron-enriched mesencephalic cultures. (A) Western blot analysis showing dephosphorylation of GSK-3β in GT1b-treated cultures. Cell lysates were analyzed by Western blot analysis with phospho-GSK-3β (Ser9) antibody at indicated time points. After membrane stripping, blots were reprobed with total GSK-3β. (B) The histogram shows quantification of phospho-GSK-3β levels. The values represent the mean ± SEM of four separate experiments; *P < 0.001, significant from non-treated control cultures (0 h) (ANOVA and Student-Newman-Keuls analyses). (C) TH-ip neurons were counted in cultures treated with 20 μg/ml GT1b for 24 h in the absence or presence of 20 μM L803-mt, GSK-3β specific inhibitor. The values represent the mean ± SEM of triplicate cultures in three to five separate samples. *P < 0.001, significant from non-treated control cultures; #P < 0.01, significant from GT1b-treated cultures (ANOVA and Student-Newman-Keuls analyses).

Back to article page