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Publication : Rule learning, visuospatial function and motor performance in the Hdh(Q92) knock-in mouse model of Huntington's disease.

First Author  Trueman RC Year  2009
Journal  Behav Brain Res Volume  203
Issue  2 Pages  215-22
PubMed ID  19445966 Mgi Jnum  J:150366
Mgi Id  MGI:3850590 Doi  10.1016/j.bbr.2009.05.006
Citation  Trueman RC, et al. (2009) Rule learning, visuospatial function and motor performance in the Hdh(Q92) knock-in mouse model of Huntington's disease. Behav Brain Res 203(2):215-22
abstractText  Among a range of genetic mouse models of Huntington's disease, knock-in models that express full-length mutant huntingtin tend to have a slower developing and less severe behavioural phenotype than transgenic models carrying truncated variations of the human gene; as a result, these more subtle full-length knock-in models have been relatively neglected for behavioural and therapeutic studies. In the current study, we show that full-length knock-in Hdh(Q92) mice exhibit marked impairments at a relatively young age in delayed alternation, a cognitive test conducted in 9-hole operant chambers classically associated with prefrontal and corticostriatal function. Additional tests of motivation, visuomotor and rotarod performance were undertaken to determine the frontal-like specificity of the impairment; aspects of sensorimotor and motivational as well as cognitive performance were deficient in Hdh(Q92/Q92) mice in comparison with their wildtype littermates by 27 months of age. The present results demonstrate that Hdh(Q92/Q92) mice do exhibit clear impairments on a range of sensory, motor, motivational and cognitive tests, provided appropriate sensitive tasks are used.
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