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. 2013 Jan 23;33(4):1391–1399. doi: 10.1523/JNEUROSCI.2231-12.2013

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Copyright © 2013 the authors 0270-6474/13/331391-09$15.00/0

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Figure 3. — Phenotypic analysis of Chi3 mice. A, Typical clinical phenotypes at the terminal stage: ataxia (left), kyphosis (middle), and clasping when held head down by the tail (right). B, Chi3 mice were maintained on the Prnp^+/+ (n = 38), Prnp^+/0 (n = 37), Prnp^0/0 (n = 12), and Prnp^+/0tga20^+/− (n = 8) allelotypes and monitored for the onset of the ataxia. Chi3Prnp^+/0 and Chi3Prnp^0/0 mice start showing coarse tremor slightly more rapidly than Chi3Prnp^+/+ (p ≤ 0.001, Mann–Whitney test), whereas most Chi3tga20^+/−Prnp^+/0 remain asymptomatic. C, The mice were killed when the following neurological symptoms were observed: feet clasping when lifted, paresis of the hind legs, and prostration. The survival of mice is dependent of Prnp status, with Chi3Prnp^+/0 and Chi3Prnp^+/+ mice surviving longer than Chi3Prnp^0/0 (p ≤ 0.001, Mann–Whitney test), whereas Chi3tga20^+/−Prnp^+/0 mice have a longer life expectancy (≥400d). D, Rotarod testing in acceleration mode of Chi3Prnp^+/0 (n = 5), Chi3tga20^+/−Prnp^+/0 (n = 5) and tga20^+/−Prnp^+/0 (n = 5) mice. Overexpression of WT PrP^c improves rotarod performance in Chi3 mice (Chi3tga20^+/−Prnp^+/0, p < 0.0001). This improvement still differs from tga20^+/−Prnp^+/0 control mice. Chi3Prnp^+/0 mice continue to deteriorate, not being able to stay on the rod from 19 weeks of age. Significant differences were tested using one-way ANOVA with Tukey's post hoc comparison.