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钙作为小脑长时程突触抑制的触发因素。

Calcium as a trigger for cerebellar long-term synaptic depression.

机构信息

Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.

出版信息

Cerebellum. 2012 Sep;11(3):706-17. doi: 10.1007/s12311-011-0314-x.

Abstract

Cerebellar long-term depression (LTD) is a form of long-term synaptic plasticity that is triggered by calcium(Ca2+) signals in the postsynaptic Purkinje cell. This Ca2+comes both from IP3-mediated release from intracellular Ca2+ stores, as well as from Ca2+ influx through voltage-gated Ca2+ channels. The Ca2+ signal that triggers LTD occurs locally within dendritic spines and is due to supralinear summation of signals coming from these two Ca2+ sources. The properties of this postsynaptic Ca2+signal can explain several features of LTD, such as its associativity, synapse specificity, and dependence on thetiming of synaptic activity, and can account for the slow kinetics of LTD expression. Thus, from a Ca2+ signaling perspective, LTD is one of the best understood forms of synaptic plasticity.

摘要

小脑长时程抑制(LTD)是一种长时程突触可塑性,由突触后浦肯野细胞中的钙(Ca2+)信号触发。这种 Ca2+既来自 IP3 介导的细胞内 Ca2+库释放,也来自通过电压门控 Ca2+通道的 Ca2+内流。触发 LTD 的 Ca2+信号在树突棘内局部发生,这是由于来自这两个 Ca2+源的信号的超线性总和。这种突触后 Ca2+信号的特性可以解释 LTD 的几个特征,如关联性、突触特异性以及对突触活动时间的依赖性,并可以解释 LTD 表达的缓慢动力学。因此,从 Ca2+信号的角度来看,LTD 是最被理解的突触可塑性形式之一。

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