Induction of neostriatal neurogenesis slows disease progression in a transgenic murine model of Huntington disease
J. Clin. Invest. Sung-Rae Cho, et al. 117:2889 doi:10.1172/JCI31778 [Go to this article.]

Figure 2
AdNoggin potentiated AdBDNF-induced neuronal addition and integration. (A) Density of BrdU⁺βIII-tubulin⁺ cells in the striatum of R6/2 and WT mice injected once at 4 wk of age with AdBDNF/AdNoggin (AdB/N), AdBDNF, AdNoggin, AdNull, or saline. (B–E) Newly generated neurons were recognized in both WT (B) and R6/2 (C–E) mice by confocal imaging of BrdU (green) colabeling with βIII-tubulin (red, B and C), DARPP-32 (red, D), or GAD67 (red, E). (F) Density of BrdU⁺ cells (green) coexpressing either DARPP-32, GAD67, enkephalin (Enk), or SP in the striatum of AdBDNF/AdNoggin-, AdBDNF-, or AdNull-injected WT and R6/2 mice. (G and H) BrdU-tagged (green) enkephalinergic (red, G) and SP (red, H) neurons in R6/2 mice. (I and J) FG injection of the globus pallidus revealed BrdU-tagged striatal projection neurons in AdBDNF/AdNoggin-injected 11-wk-old WT (I) and R6/2 (J) mice. *P < 0.05, **P < 0.01, ***P < 0.001, 1-way ANOVA followed by post-hoc Bonferroni t tests. Arrows denote double-labeled cells. Scale bars: 10 μm.