Figure 3.

Preketamine treatment with a subtherapeutic dose of lithium potentiates the activation of mammalian target of rapamycin (mTOR)/brain-derived neurotrophic factor (BDNF)-tropomyosin-related kinase B (TrkB) signaling pathways induced by acute challenge with a low dose of ketamine. Mice were pretreated with 600mg/L of lithium for 3 weeks, and brain tissues were collected 60 minutes after a single injection of saline (lithium alone group) or a very low dose (2.5mg/kg) of ketamine (lithium + ketamine group). Typical Western blots and quantified results are shown. The phosphorylation levels of mTOR, P70S6K, eukaryotic elongation factor-2 (eEF2), and the expression of postsynaptic density protein 95 (PSD95) (a), as well as the phosphorylation levels of TrkB, Akt, extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3β (GSK-3β) (b) in the prefrontal cortex (PFC) were normalized to the levels of total protein or β-actin and expressed as percentage of control group. Data are mean±SEM (n =4–8). ++P<.01, t test; *P<.05, **P<.01, according to Student–Newman–Keuls multiple comparison test after a 1-way analysis of variance (ANOVA). P, phosphorylated protein; T, total protein; US, unstressed.