Motor dysfunction and neuropathology (including striatal neuron loss) in 17-month-old Tet/HD94 mice. A, B, Rota-Rod analysis of 17-month-old control (open squares; n = 20) and Tet/HD94 (filled circles; n=21) mice. Values in A represent mean ± SEM time spent on Rota-Rod, per daily trial and genotype (see Material and Methods) (^*p < 0.01; ^**p < 0.005). Values in B represent mean ± SEM of the latencies to fall in the eight trials per genotype (^*p < 0.01). C, Immunohistochemistry with anti-N-terminal mutant-htt (CAG53b) antibody revealed the presence of aggregates in the forebrains of Tet/HD94 mice. Scale bar, 20 μm. D, Immunoelectron microscopy analysis of a CAG53b-stained inclusion from a Tet/HD94 mouse. The inset in D corresponds to a 2.0× magnification of the indicated area, showing that inclusions are formed by randomly oriented filamentous structures. Scale bar, 1 μm. E, F, Striatal atrophy can be observed in coronal sections like those stained with anti-Neu-N antibody from control (E) and Tet/HD94 (F) mice. Scale bar: (in E) E, F, 500 μm. G, Stereological measurement of striatal size for control (open bar; n = 4) and Tet/HD94 (filled bar; n = 4) mice. H, Stereological analysis of number (N.) of striatal neurons in control (open bar; n = 4) and Tet/HD94 (filled bar; n = 4) as determined by Neu-N staining. ^*p < 0.01. Error bars indicate SE.