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树突棘中的钙信号传导。

Calcium signaling in dendritic spines.

机构信息

Department of Neurobiology, Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale School of Medicine, New Haven, Connecticut 06520, USA.

出版信息

Cold Spring Harb Perspect Biol. 2012 Apr 1;4(4):a005686. doi: 10.1101/cshperspect.a005686.

Abstract

Calcium (Ca(2+)) is a ubiquitous signaling molecule that accumulates in the cytoplasm in response to diverse classes of stimuli and, in turn, regulates many aspects of cell function. In neurons, Ca(2+) influx in response to action potentials or synaptic stimulation triggers neurotransmitter release, modulates ion channels, induces synaptic plasticity, and activates transcription. In this article, we discuss the factors that regulate Ca(2+) signaling in mammalian neurons with a particular focus on Ca(2+) signaling within dendritic spines. This includes consideration of the routes of entry and exit of Ca(2+), the cellular mechanisms that establish the temporal and spatial profile of Ca(2+) signaling, and the biophysical criteria that determine which downstream signals are activated when Ca(2+) accumulates in a spine. Furthermore, we also briefly discuss the technical advances that made possible the quantitative study of Ca(2+) signaling in dendritic spines.

摘要

钙(Ca(2+))是一种普遍存在的信号分子,它在细胞质中积累,以响应各种刺激,进而调节细胞功能的许多方面。在神经元中,钙(Ca(2+))内流响应动作电位或突触刺激触发神经递质释放,调节离子通道,诱导突触可塑性,并激活转录。在本文中,我们讨论了调节哺乳动物神经元中 Ca(2+)信号的因素,特别关注树突棘内的 Ca(2+)信号。这包括考虑 Ca(2+)进入和离开的途径、建立 Ca(2+)信号时间和空间特征的细胞机制,以及决定 Ca(2+)在脊柱中积累时哪些下游信号被激活的物理标准。此外,我们还简要讨论了使树突棘中 Ca(2+)信号的定量研究成为可能的技术进展。

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