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. 2013 Apr 17;33(16):6990–7002. doi: 10.1523/JNEUROSCI.4998-12.2013

Figure 4.

Figure 4.

The acute antidepressant-like effects of ketamine requires eEF2 kinase activity. A, B, Immunoblot analysis of phospho-eEF2 and total eEF2 expression in total protein lysates from prefrontal cortex or hippocampus in eEF2 kinase knock-outs (KOs) or wild-type (WT) littermate controls reveals that phosphorylation of eEF2 is negligible after loss of eEF2 kinase (cortex, p = 0.0054; hippocampus, p = 0.0005) (n = 5/group). C, Immunoblot analysis of BDNF expression in WT mice and their eEF2 kinase KO littermates treated for 30 min with vehicle or ketamine (5 mg/kg) illustrates that BDNF expression does not increase in hippocampus after acute ketamine treatment in eEF2 kinase KO mice (p = 0.138) (n = 4/group). D, Acute ketamine treatment (30 min; 5 mg/kg) decreases immobility in WT animals compared with vehicle-treated mice in the forced swim test. In contrast, their eEF2K KO littermates do not respond to application of ketamine (ANOVA F(1,25) = 4.530, Tukey's post hoc test, p < 0.05; n = 7–8 group). E, eEF2 kinase KO mice do not show rapid antidepressant responses to ketamine administration in the novelty suppressed feeding (NSF) paradigm. WT control mice and their eEF2K KO littermates were administered vehicle or ketamine (5.0 mg/kg) intraperitoneally. In NSF test, latency to feed was recorded 30 min after ketamine injection. Ketamine-treated WT control mice show decreased latency to feed (ANOVA, F(3,29) = 6.487, p = 0.0017 for treatment; with Tukey's post hoc, p < 0.05); whereas ketamine-treated eEF2K KO animals show no change in latency to acquire food. F, Post-test for the 30 min NSF test demonstrating that all groups show comparable appetites.