کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4314660 | 1290044 | 2009 | 8 صفحه PDF | دانلود رایگان |
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 HdhQ92 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 HdhQ92/Q92 mice in comparison with their wildtype littermates by 27 months of age. The present results demonstrate that HdhQ92/Q92 mice do exhibit clear impairments on a range of sensory, motor, motivational and cognitive tests, provided appropriate sensitive tasks are used.
Journal: Behavioural Brain Research - Volume 203, Issue 2, 5 November 2009, Pages 215–222