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. Author manuscript; available in PMC: 2009 Aug 19.
Published in final edited form as: J Neurosci. 2009 Feb 18;29(7):2193–2204. doi: 10.1523/JNEUROSCI.5473-08.2009

Fig. 2. Mutant huntingtin exacerbates neuronal dysfunction following stroke injury.

Fig. 2

A) Assessment of motor function in 1.5 month old YAC128 (HD53) and WT mice 24 hrs post ischemia-induced injury reveals the presence of mhtt delays the recover of motor function in YAC128 (HD53) mice compared to WT (p<0.05). No difference between genotypes is observed for baseline gross sensorimotor behavior 2 hrs post stroke injury. B) Percent recovery from MCAO is significantly reduced in YAC128 (HD53) mice vs. WT (p<0.01). In contrast to WT mice, which demonstrate an improvement in motor function 24 hrs post ischemia (23%), YAC128 (HD53) continue to perform poorly (−4%). C) Representative images of infarct volume in YAC128 (HD53) vs. WT coronal sections reveal the ischemic-induced damage by TTC staining. Quantification of lesion volume demonstrates a 39% increase in YAC128 (HD53) compared to control which approaches statistical significance (p<0.09). Lesion volume is ± SEM. *p<0.05; **p<0.01.