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[小脑长期抑制:一种学习与记忆的机制]

[Cerebellar long-term depression: a mechanism for learning and memory].

作者信息

Vigot Réjan

机构信息

Division of Speciation Mechanisms I, National Institute for Basic Biology, Nishigonaka 38, Myodaiji-cho, Okazaki 444-8585, Japon.

出版信息

Med Sci (Paris). 2003 Apr;19(4):437-41. doi: 10.1051/medsci/2003194437.

DOI:10.1051/medsci/2003194437
PMID:12836216
Abstract

It is commonly thought that a persistent change in the efficacy of the synaptic transmission is the basic mechanism underlying learning and memory. The cerebellum, key structure of the motor function, exhibits a synaptic plasticity named cerebellar long-term depression or LTD. This phenomenon appears in the Purkinje cell when the two main excitatory inputs (one consists of the parallel fibers which relay information on the task to accomplish and the other one includes the climbing fiber which conveys error signals) are activated in combination, resulting in a persistent decrease of the efficacy of the parallel fiber-Purkinje cell synapse. Studies made in the last 20 years show that activation of ionotropic and metabotropic glutamate receptors triggers complex signal transduction processes, leading to the phosphorylation and the internalization of AMPA receptors, a subtype of glutamatergic receptors. The aim of this paper is firstly to present mechanisms involved in LTD induction and maintenance. The second part introduces briefly experimental data that show that LTD is indeed strongly associated with motor learning. Recent studies on the involvement of the cerebellum in cognitive tasks also suggest that LTD may play some role other than that in the sole motor learning.

摘要

人们普遍认为,突触传递效能的持续变化是学习和记忆的基本机制。小脑作为运动功能的关键结构,表现出一种名为小脑长时程抑制(LTD)的突触可塑性。当两个主要的兴奋性输入(一个由传递关于要完成任务信息的平行纤维组成,另一个包括传递误差信号的攀缘纤维)联合激活时,这种现象出现在浦肯野细胞中,导致平行纤维 - 浦肯野细胞突触效能的持续降低。过去20年的研究表明,离子型和代谢型谷氨酸受体的激活触发复杂的信号转导过程,导致AMPA受体(一种谷氨酸能受体亚型)的磷酸化和内化。本文的目的首先是介绍LTD诱导和维持所涉及的机制。第二部分简要介绍了实验数据,这些数据表明LTD确实与运动学习密切相关。最近关于小脑参与认知任务的研究也表明,LTD可能在除单纯运动学习之外还发挥一些作用。

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1
[Cerebellar long-term depression: a mechanism for learning and memory].[小脑长期抑制:一种学习与记忆的机制]
Med Sci (Paris). 2003 Apr;19(4):437-41. doi: 10.1051/medsci/2003194437.
2
Role of presynaptic kainate receptors at parallel fiber-purkinje cell synapses in induction of cerebellar LTD: interplay with climbing fiber input.突触前海人藻酸受体在平行纤维-浦肯野细胞突触诱导小脑长时程抑制中的作用:与攀缘纤维输入的相互作用。
J Neurophysiol. 2009 Aug;102(2):965-73. doi: 10.1152/jn.00269.2009. Epub 2009 Jun 17.
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Deficient cerebellar long-term depression and impaired motor learning in mGluR1 mutant mice.代谢型谷氨酸受体1(mGluR1)突变小鼠的小脑长时程抑制缺陷及运动学习受损。
Cell. 1994 Oct 21;79(2):377-88.
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Induction of cerebellar long-term depression requires activation of calcineurin in Purkinje cells.小脑长时程抑制的诱导需要浦肯野细胞中钙调神经磷酸酶的激活。
Neuropharmacology. 2007 Jun;52(8):1663-70. doi: 10.1016/j.neuropharm.2007.03.011. Epub 2007 Apr 4.
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[Functional analysis of molecules involved in synaptic plasticity in the cerebellum].[小脑突触可塑性相关分子的功能分析]
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alphaCaMKII Is essential for cerebellar LTD and motor learning.α钙调蛋白激酶II对小脑长时程抑制和运动学习至关重要。
Neuron. 2006 Sep 21;51(6):835-43. doi: 10.1016/j.neuron.2006.08.013.
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Cerebellar long-term depression requires dephosphorylation of TARP in Purkinje cells.小脑长时程抑制需要浦肯野细胞中 TARP 的去磷酸化。
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Systems biology perspectives on cerebellar long-term depression.小脑长时程抑制的系统生物学观点。
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Induction of long-term depression and phosphorylation of the delta2 glutamate receptor by protein kinase C in cerebellar slices.蛋白激酶C在小脑切片中诱导δ2谷氨酸受体的长时程抑制和磷酸化
Eur J Neurosci. 2005 Oct;22(7):1817-20. doi: 10.1111/j.1460-9568.2005.04319.x.
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Synaptic plasticity in the cerebellar cortex and its role in motor learning.小脑皮质中的突触可塑性及其在运动学习中的作用。
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