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. 2012 Oct 17;32(42):14592–14601. doi: 10.1523/JNEUROSCI.0539-12.2012

Figure 3.

Figure 3.

MPTP-depleted TH in the striatum is recovered by sFKN. Both hemispheres were rapidly dissected 7 days following the last MPTP or saline injections for biochemical analysis. a, Western blot analysis revealed that MPTP exposure significantly reduced the availability of TH in the striatum (three-way ANOVA; F(1, 23) = 34.42, ★★★p < 0.001). Additionally, FKN−/− sham animals had no distinguishable difference in TH production compared to WT-Sham mice. CX3CL1−/− mice expressing sFKN in the SNpc had an attenuated loss of TH compared to mFKN (Tukey's HSD; ***p < 0.001) and GFP (Tukey's HSD; ###p < 0.001) expressing mice. There were no significant differences between CX3CL1−/− mice expressing either mFKN or GFP (Tukey's HSD; p = 0.627). b–g, Representative immunostaining in the striatum shows progressive loss of TH for FKN−/− sham (b), WT-Sham (c), WT-MPTP (d), sFKN (e), mFKN (f), and GFP (g) groups. Data are presented as the mean band density ratio (n = 5 per group) of TH to actin as a percentage WT-Sham ± SEM. Scale bars, 200 μm.