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小脑长期抑制的细胞机制。

Cellular mechanisms of long-term depression in the cerebellum.

作者信息

Linden D J, Connor J A

机构信息

Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.

出版信息

Curr Opin Neurobiol. 1993 Jun;3(3):401-6. doi: 10.1016/0959-4388(93)90133-j.

DOI:10.1016/0959-4388(93)90133-j
PMID:8369630
Abstract

Cerebellar long-term depression is a persistent, input-specific attenuation of the parallel fiber-Purkinje neuron synapse induced by co-activation of parallel fibers and climbing fibers. This phenomenon endows the Purkinje neuron with a powerful associative computational ability. Recent investigations have provided strong evidence that two mechanisms, Ca2+ influx via voltage-gated channels, and stimulation of protein kinase C via metabotropic receptor activation, are required for induction of long-term depression. In addition, two other mechanisms, Na+ influx via AMPA receptors, and stimulation of a nitric oxide/cGMP cascade may also be involved in this process.

摘要

小脑长期抑郁是平行纤维与浦肯野神经元突触在平行纤维和攀缘纤维共同激活时所诱导的一种持续性、输入特异性减弱。这种现象赋予浦肯野神经元强大的联合计算能力。最近的研究提供了强有力的证据,表明诱导长期抑郁需要两种机制,即通过电压门控通道的Ca2+内流和通过代谢型受体激活对蛋白激酶C的刺激。此外,另外两种机制,即通过AMPA受体的Na+内流和一氧化氮/cGMP级联反应的刺激也可能参与这一过程。

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1
Cellular mechanisms of long-term depression in the cerebellum.小脑长期抑制的细胞机制。
Curr Opin Neurobiol. 1993 Jun;3(3):401-6. doi: 10.1016/0959-4388(93)90133-j.
2
Induction of cerebellar long-term depression in culture requires postsynaptic action of sodium ions.培养物中小脑长时程抑制的诱导需要钠离子的突触后作用。
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3
An NMDA receptor/nitric oxide cascade is involved in cerebellar LTD but is not localized to the parallel fiber terminal.N-甲基-D-天冬氨酸受体/一氧化氮级联反应参与小脑长时程抑制,但并不局限于平行纤维终末。
J Neurophysiol. 2005 Dec;94(6):4281-9. doi: 10.1152/jn.00661.2005. Epub 2005 Aug 24.
4
Beyond parallel fiber LTD: the diversity of synaptic and non-synaptic plasticity in the cerebellum.超越平行纤维长时程抑制:小脑突触和非突触可塑性的多样性
Nat Neurosci. 2001 May;4(5):467-75. doi: 10.1038/87419.
5
Receptors, second messengers and protein kinases required for heterosynaptic cerebellar long-term depression.异突触性小脑长时程抑制所需的受体、第二信使和蛋白激酶。
Neuropharmacology. 2001;40(1):148-61. doi: 10.1016/s0028-3908(00)00107-6.
6
Long-Term Depression of Intrinsic Excitability Accompanied by Synaptic Depression in Cerebellar Purkinje Cells.小脑浦肯野细胞中内在兴奋性的长期抑制伴随着突触抑制
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Inositol-1,4,5-trisphosphate receptor-mediated Ca mobilization is not required for cerebellar long-term depression in reduced preparations.在简化制备中,小脑长时程抑制并不需要肌醇-1,4,5-三磷酸受体介导的钙动员。
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Roles of phospholipase Cbeta4 in synapse elimination and plasticity in developing and mature cerebellum.磷脂酶Cβ4在发育中和成熟小脑中突触消除及可塑性中的作用
Mol Neurobiol. 2001 Feb;23(1):69-82. doi: 10.1385/MN:23:1:69.
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Spatial distribution of synaptically activated sodium concentration changes in cerebellar Purkinje neurons.小脑浦肯野神经元中突触激活的钠浓度变化的空间分布。
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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]
Tanpakushitsu Kakusan Koso. 2008 Mar;53(4 Suppl):544-8.

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