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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Nat Neurosci. 2014 Jan 26;17(3):367–376. doi: 10.1038/nn.3636

Figure 6. Loss of LRRK2 causes alteration of PKA-dependent phosphorylation of GluR1 in young and aged mice.

Figure 6

(a) Western blot analysis of pS845 GluR1, total GluR1 and LRRK2 expression in the forebrain homogenates of P2, P5, P15, and P30 LRRK2+/+ and LRRK2−/− mice. (b) Quantification analysis of pS845 GluR1 levels normalized to total GluR1 levels derived of three independent experiments. Data represent mean ± SEM. Unpaired t-test, t(4)=0.5791, 6.282, 3.576, and 1.061, respectively. *p<0.05, **p<0.01. (c) Western blot analysis of GluR1 and PSD95 in the S1 and PSD fractions of P15 LRRK2+/+ and LRRK2−/− mouse brains. (d,e) Quantification analysis of GluR1 levels in the PSD versus S1 fractions of brain extracts (d), as well as GluR1 levels versus PSD95 levels in the PSD fraction of brain extracts (e). n=3 per genotype. Data represent mean ± SEM. Unpaired t-test, t(4)=4.218 (d) and 4.206 (e). *p<0.05. (f) Western blot analysis of pS845 and total GluR1 in the striatum of P21 LRRK2+/+ and LRRK2−/− mice after treated with saline (0) or Drd1 agonist SKF81297 at 2 and 10mg per kg bodyweight. Actin was used as the loading control. (g,h) Quantification analysis of pS845 GluR1 ratio in the striatal tissues of P21 (g) and 18-month-old mice (h) treated with SKF81297. n=4 per genotype per treatment. Data represent mean ± SEM. Unpaired t-test. t(8)=2.501, 2.177, and 4.605 in (g). t(6)=3.703 and 4.401 in (h). *p<0.05, **p<0.01. The full-length images of Fig. 6a,c,f are shown in Supplementary Fig. 6h-j.