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围绕运动学习中的长时程抑制假说。

Around LTD hypothesis in motor learning.

作者信息

Hirano Tomoo

机构信息

Department of Biophysics, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, 606-8502, Japan,

出版信息

Cerebellum. 2014 Oct;13(5):645-50. doi: 10.1007/s12311-014-0581-4.

DOI:10.1007/s12311-014-0581-4
PMID:24974094
Abstract

Long-term depression (LTD) at parallel fiber-Purkinje neuron synapses has been regarded as a primary cellular mechanism for motor learning. However, this hypothesis has been challenged. Demonstration of normal motor learning under LTD-suppressed conditions suggested that motor learning can occur without LTD. Synaptic plasticity mechanisms other than LTD have been found at various synapses in the cerebellum. Animals may achieve motor learning using several types of synaptic plasticity in the cerebellum including LTD.

摘要

平行纤维-浦肯野神经元突触处的长时程抑制(LTD)被认为是运动学习的主要细胞机制。然而,这一假说受到了挑战。在LTD抑制条件下正常运动学习的证明表明,运动学习可以在没有LTD的情况下发生。在小脑的各种突触中发现了LTD以外的突触可塑性机制。动物可能利用小脑包括LTD在内的几种类型的突触可塑性来实现运动学习。

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本文引用的文献

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Role of granule-cell transmission in memory trace of cerebellum-dependent optokinetic motor learning.小脑依赖型视动运动学习记忆痕迹中颗粒细胞传递的作用。
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小脑绒球内β-和α2-肾上腺素受体对前庭眼反射和视动反应的差异调节。
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Compromised Survival of Cerebellar Molecular Layer Interneurons Lacking GDNF Receptors GFRα1 or RET Impairs Normal Cerebellar Motor Learning.缺乏胶质细胞源性神经营养因子受体GFRα1或RET的小脑分子层中间神经元存活受损,会损害正常的小脑运动学习。
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T-type channel blockade impairs long-term potentiation at the parallel fiber-Purkinje cell synapse and cerebellar learning.T 型通道阻断会损害平行纤维-浦肯野细胞突触的长时程增强和小脑学习。
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Cerebellar Purkinje cell activity drives motor learning.小脑浦肯野细胞活动驱动运动学习。
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Long-term potentiation of inhibitory synaptic transmission onto cerebellar Purkinje neurons contributes to adaptation of vestibulo-ocular reflex.小脑浦肯野神经元抑制性突触传递的长时程增强有助于前庭眼反射的适应。
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Long-term depression and other synaptic plasticity in the cerebellum.小脑的长期抑郁和其他突触可塑性。
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