کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6259179 | 1612991 | 2013 | 6 صفحه PDF | دانلود رایگان |
The physiological and pathophysiological role of the cerebellum in neuromotor performance and gait is a prominent research topic in contemporary brain research. However, it has proven difficult to measure subtle neuromotor changes and cerebellar dysfunction in laboratory rodents with some of the common behavioural assays. Rotarod assays and gait analyses have been used extensively as indicators of neuromotor performance, and more specifically, cerebellar function. Standard rotarod procedures fail to reveal subtle motor alterations, whereas automated gait analysis could be more sensitive in this respect. In the present study, we compared detailed treadmill gait analysis to the standard accelerating rotarod assay in its ability to reveal neuromotor alterations in mice with small bilateral lesions in the cerebellar cortex. This small lesion model showed no readily observable signs of ataxia or abnormal activity. In the rotarod test, cerebellar-lesioned mice performed at the level of control animals, and basic gait parameters were not altered. However, cerebellar-lesioned mice did show increased front base-width and hind stride length variability, as well as increased stride length incongruity between different paws. We conclude that small cerebellar lesions lead to increased gait variability as it does in humans with cerebellar dysfunction. Treadmill gait analysis is better suited than accelerating rotarod assays to measure such subtle neuromotor defects.
⺠Bilateral lesions of the cerebellar cortex were electrolytically produced in mice. ⺠Cerebellar lesioned mice showed no overt signs of ataxia or abnormal ambulation. ⺠Accelerating rotarod did not distinguish cerebellar lesioned mice from sham controls. ⺠Treadmill gait analysis distinguished cerebellar lesioned mice from sham controls. ⺠Cerebellar lesions evoked an increase of gait variability in mice.
Journal: Behavioural Brain Research - Volume 241, 15 March 2013, Pages 32-37