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. 2017 Feb 13;8:14405. doi: 10.1038/ncomms14405

Figure 8. CK2α′ heterozygosity ameliorates biochemical and neurobiological defects in KI175 HD mice.

Figure 8

(a,b) Dendrite spine number and morphology of MSNs in the dorsal-striatum of KIQ175 and KIQ175/CK2α′+/− at 6 months. Scale bar, 10 μm. Error bars indicate mean±s.e.m., (n=12 cells/animal, 3 animals/genotype). Unpaired t-test *P<0.05, **P<0.01. (c) Excitatory synapse input in the dorsal striatum. (d) Immunostaining of the cortico-striatal pre-synaptic marker (VGlut1, red), the thalamo-striatal pre-synaptic marker (VGlut2, red) and the post-synaptic marker PSD95 (green) in the dorsal-striatum of KIQ175, WT, KIQ175/CK2α′+/−, and CK2α′+/− at 6 months. Scale bar, 10 μM. (e) Quantification of VGlut1-PSD95 and (f) VGlut2-PSD95 co-localized synaptic puncta from B. Error bars indicate mean±s.e.m., (n=3 animals per genotype, 3 sections per animal, 15 sections per scan). Unpaired t-test *P<0.05, **P<0.01. (g,h) Size and body weight of KIQ175 (n=6), WT (n=8), KIQ175/CK2α′+/− (n=11) and CK2α′+/− (n=11) at 6 months. Error bars indicate±s.e.m. Unpaired t-test *P<0.05.