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The somatotopic organisation of the cortex, and the topographically organised afferent and efferent connections of the striatum mirror the diverse nature of deficits observed following striatal lesions in the rat (46). For example, regional striatal lesions have demonstrated the differential effects of the lateral and medial striatal contribution to motor functions (47). Dorsolateral striatal lesions selectively produce skilled forelimb deficits, while dorsoventral striatal lesions impair both skilled forelimb use and tongue reaching.

Van der Burg JM, Bacos K, Wood NI et al (2008) Increased metabolism in the R6/2 17 mouse model of Huntington’s disease. Neurobiol Dis 29: 41–51. Weydt P, Pineda VV, Torrence AE et al (2006) Thermoregulatory and metabolic defects in Huntington’s disease transgenic mice implicate PGC-1alpha in Huntington’s disease neurodegeneration. Cell Metab 4: 349–362. Bolivar VJ, Manley K, Messer A (2003) Exploratory activity and fear conditioning abnormalities develop early in R6/2 Huntington’s disease transgenic mice.

The time taken to turn to face downwards (t. turn) is measured, in addition to the total time to complete the task (t.  descend), following the turn. We found a marked increase in the total time to complete the task at 4 months in the CAG140 KI mice (45) and this has now also been observed in several lines of different repeat length R6/2 mice (Cummings et al. submitted). 6. Conclusion In conclusion, both simple but labor intensive (climbing cage, pole test) and almost or fully automated tests (open field, running wheels) can be used to detect early motor deficits in mouse models of HD.

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