Lithium treatment inhibited the GSK-3 signaling pathway in the mouse hippocampus after TMT treatment.

<p>Mice were treated with lithium chloride (50 mg/kg, i.p.) 0 and 24 h after TMT (2.6 mg/kg, i.p.) administration and hippocampi were dissected at various time–points for Western blot analysis. (A) Bar graphs show significant increases in the inhibitory phosphorylation of GSK-3α (Ser²¹) in the hippocampus 2 and 4 days post-treatment. (B) Bar graphs show a significant increase in the inhibitory phosphorylation of GSK-3β (Ser⁹) in the hippocampus 2 days post-treatment. To quantify the inhibitory phosphorylation of either GSK-3α or GSK-3β, phosphorylated forms were normalized to either total GSK-3α or GSK-3β. (C) Bar graphs show a significant increase in β–catenin expression in the hippocampus 4 days post-treatment. For normalization of β–catenin expression, the membranes were reprobed with β-actin antibody. Immunoblot images for phospho-GSK-3α (Ser²¹), total GSK-3α, phospho-GSK-3β (Ser⁹), total GSK-3β, β–catenin and β-actin are shown in the Supporting Information (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070356#pone.0070356.s001" target="_blank">Fig. S1</a>). The data are reported as the means±SEM (<i>n</i> = 3 per group). *<i>p</i><0.05 <i>vs.</i> TMT-treated mice. TMT, TMT-treated mice; TMT+Li, TMT+lithium-treated mice.