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首页> 外文期刊>The European Journal of Neuroscience >p53 inactivation leads to impaired motor synchronization in mice.
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p53 inactivation leads to impaired motor synchronization in mice.

机译:p53失活导致小鼠运动同步受损。

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摘要

We have combined genetic and pharmacological approaches to investigate the behavioural consequences of inactivation of the murine p53 protein. Our behavioural analysis revealed that p53-null mice (p53KO) exhibit a very specific and significant motor deficit in rapid walking synchronization. This deficit, observed using the rotarod test, was the only behavioural defect of p53KO mice. We demonstrated that it was not due to an increase in neuronal number or abnormal connectivity in the olivo-cerebellar system, thought to control motor synchronization. In order to test the role of p53 in the central nervous system, we injected a pharmacological inhibitor of p53 activation, pifithrin-alpha, into the cerebellum of wild-type mice. This treatment mimicked the walking synchronization deficit of p53KO mice, suggesting that presence of p53 protein in the cerebellum is necessary to execute this synchronization of walking. Our investigation reveals a functional role of cerebellar p53 protein in adult walking synchronization.
机译:我们已经结合了遗传和药理学方法来研究灭活鼠p53蛋白的行为后果。我们的行为分析表明,p53无效的小鼠(p53KO)在快速步行同步过程中表现出非常特异性和显着的运动缺陷。使用旋转脚架试验观察到的这种缺陷是p53KO小鼠的唯一行为缺陷。我们证明这不是由于小脑小脑系统中神经元数目的增加或连接异常,而被认为是控制运动同步的原因。为了测试p53在中枢神经系统中的作用,我们向野生型小鼠小脑中注射了p53活化的药理抑制剂pifithrin-alpha。这种治疗模仿了p53KO小鼠的步行同步缺陷,表明小脑中p53蛋白的存在对于执行这种步行同步是必要的。我们的研究揭示了小脑p53蛋白在成人步行同步中的功能作用。

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