Figure 5

Rapamycin treatment normalizes Kv1.1 protein levels in NS-Pten KO mice. WT and NS-Pten KO mice were treated with vehicle or rapamycin (10 mg/kg i.p.) for 5 days per week for 2 weeks, either during postnatal weeks 4 and 5 (A,B; early treatment) or during postnatal weeks 9 and 10 (C,D; late treatment). Tissue was collected for western blotting one day after the last treatment. (A) Representative western blots from whole hippocampal homogenates from early control (naïve and vehicle-treated) and rapamycin-treated WT and NS-Pten KO mice probed with antibodies against Kv1.1, Kv1.2, Kv1.4, and actin are shown. Full-length blots are presented in Supplemental Fig. 2. (B) Quantification of western blots showed that Kv1.1 protein levels were significantly higher in NS-Pten KO compared to WT mice in the control group. Early rapamycin treatment suppressed Kv1.1 protein levels in NS-Pten KO mice to WT levels. No significant changes in Kv1.2 or Kv1.4 protein levels were found between NS-Pten KO and WT mice regardless of treatment group. n = 7–16 mice/group; ***p < 0.001 by one-way ANOVA with Tukey’s post-hoc test; errors bars are ± SEM. (C) Representative western blots from whole hippocampal homogenates from late control (naïve and vehicle-treated) and rapamycin-treated WT and NS-Pten KO mice probed with antibodies against Kv1.1, Kv1.2, Kv1.4, and actin are shown. Full-length blots are presented in Supplemental Fig. 2. (D) Quantification of western blots showed that Kv1.1 protein levels were significantly higher in NS-Pten KO compared to WT mice in the control group. Late rapamycin treatment suppressed Kv1.1 protein levels in NS-Pten KO mice to WT levels. No significant changes in Kv1.2 or Kv1.4 protein levels were found between NS-Pten KO and WT mice regardless of treatment group. n = 6–14 mice/group; *p < 0.05, ***p < 0.001 by one-way ANOVA with Tukey’s post-hoc test; errors bars are ± SEM.