Assessment of gait and sensorimotor deficits in the D1CT-7 mouse model of Tourette syndrome

步态 跨步 心理学 神经科学 抽动秽语综合征 步态分析 运动行为 物理医学与康复 医学 精神科
作者
Stephen C. Fowler,Laura J. Mosher,Sean C. Godar,Marco Bortolato
出处
期刊:Journal of Neuroscience Methods [Elsevier]
卷期号:292: 37-44 被引量:27
标识
DOI:10.1016/j.jneumeth.2017.01.009
摘要

Tourette syndrome (TS) is a neurodevelopmental disorder characterized by multiple motor and phonic tics. While TS patients have been also shown to exhibit subtle abnormalities of sensorimotor integration and gait, animal models of this disorder are seldom tested for these functions. To fill this gap, we assessed gait and sensorimotor integration in the D1CT-7 mouse, one of the best-validated animal models of TS. D1CT-7 mice exhibit spontaneous tic-like manifestations, which, in line with the clinical phenomenology of TS, are markedly exacerbated by environmental stress. Thus, to verify whether stress may affect sensorimotor integration and gait functions in D1CT-7 mice, we subjected these animals to a 20-min session of spatial confinement, an environmental stressor that was recently shown to worsen tic-like manifestations. Immediately following this manipulation (or no confinement, for controls), animals were subjected to either the sticky-tape task, to test for sensorimotor integration; or a 60-min session in an open field (42 × 42 cm) force-plate actometer for gait analysis. Gait analyses included spatial, temporal, and dynamic (force) parameters. D1CT-7 mice displayed a longer latency to remove a sticky tape, indicating marked impairments in sensorimotor integration; furthermore, these mutants exhibited shortened stride length, increased stride rate, nearly equal early-phase velocity, and higher late-phase velocity. D1CT-7 mice also ran with greater force amplitude than wild-type (WT) littermates. None of these phenotypes was worsened by spatial confinement. These results highlight the potential importance of testing sensorimotor integration and gait functions as a phenotypic correlate of cortical connectivity deficits in animal models of TS.
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