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. 2020 Jul 30;11(7):569. doi: 10.1038/s41419-020-02775-5

Fig. 5. Striatal RTP801 knockdown preserves motor learning in symptomatic R6/1 mouse.

Fig. 5

a GFP immunofluorescence confirmed the transduction of AAV-shCtr and AAV-shRTP801 in 9-week-old WT and R6/1 mice striatal cells. A secondary control was performed without the incubation of primary antibody (anti-GFP). Scale bar 450 μm. b Striatal lysates of WT and R6/1 injected with AAV-shCtr (n = 6 WT and n = 6 R6/1) or AAV-shRTP801 (n = 6 WT and n = 7 R6/1) were subjected to WB. Membranes were probed against RTP801, GFP, and actin as a loading control. Graph show the densitometric quantification of RTP801 signal. Data are shown as a mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (*P < 0.05 vs. WT AAV-shCtr #P < 0.05 vs. R6/1 AAV-shCtr). c Five weeks after adeno-associated transduction, motor learning was assessed in the same animals by the accelerating rotarod (n = 8 WT-shCtr, n = 8 WT shRTP801, n = 9 R6/1-shCtr, n = 9 R6/1-shRTP801). The graph shows the latency to fall as the mean of three trials tested each day. Values are expressed as mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (*P < 0.05, **P < 0.01, and ***P < 0.001 R6/1-shCtr vs. WT-shCtr and #P < 0.05 R6/1-shRTP801 vs. R6/1-shCtr).