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小脑对空间导航的贡献:对潜在机制的新见解。

Cerebellar contribution to spatial navigation: new insights into potential mechanisms.

作者信息

Lefort Julie M, Rochefort Christelle, Rondi-Reig Laure

机构信息

CNRS, UMR 8246, Neuroscience Paris Seine, Institut de Biologie Paris Seine(IBPS), Cerebellum, Navigation and Memory Team, Paris, France.

出版信息

Cerebellum. 2015 Feb;14(1):59-62. doi: 10.1007/s12311-015-0653-0.

Abstract

The contribution of the cerebellum to the non-motor aspects of spatial navigation is now established, but the mechanisms of its participation remain unclear. The L7-PKCI mouse model, in which inhibited PKC activity suppresses parallel fiber-Purkinje cell long-term depression (LTD), provides the opportunity to study their spatial abilities in the absence of any motor impairment. L7-PKCI mice are deficient in the spatial but not the cued version of the watermaze task. Their performances are preserved when alleys guide their trajectories in the starmaze task, suggesting that cerebellar PKC-dependent mechanisms are required for the production of an optimal trajectory toward a goal. Furthermore, electrophysiological recordings in freely moving L7-PKCI mice revealed that their hippocampal place cell properties are affected when they have to rely on self motion information: in the absence of external information as well as in a conflicting situation between self-motion and external information. This suggests that the cerebellum is involved in the processing of self-motion information and is required for the construction of the spatial representation in the hippocampus.

摘要

小脑对空间导航非运动方面的贡献现已明确,但它参与其中的机制仍不清楚。在L7-PKCI小鼠模型中,抑制蛋白激酶C(PKC)的活性会抑制平行纤维-浦肯野细胞长时程抑制(LTD),这为研究它们在没有任何运动障碍情况下的空间能力提供了机会。L7-PKCI小鼠在水迷宫任务的空间版本而非线索版本中表现不佳。当在星状迷宫任务中通道引导它们的轨迹时,它们的表现得以保留,这表明小脑依赖PKC的机制对于产生朝向目标的最佳轨迹是必需的。此外,对自由活动的L7-PKCI小鼠进行的电生理记录显示,当它们必须依靠自身运动信息时,其海马位置细胞特性会受到影响:在没有外部信息以及在自身运动和外部信息之间存在冲突的情况下。这表明小脑参与自身运动信息的处理,并且是海马体中空间表征构建所必需的。

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The cerebellum: a new key structure in the navigation system.小脑:导航系统中的新关键结构。
Front Neural Circuits. 2013 Mar 13;7:35. doi: 10.3389/fncir.2013.00035. eCollection 2013.
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