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钙离子与突触可塑性。

Ca2+ and synaptic plasticity.

作者信息

Cavazzini Michele, Bliss Tim, Emptage Nigel

机构信息

Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK.

出版信息

Cell Calcium. 2005 Sep-Oct;38(3-4):355-67. doi: 10.1016/j.ceca.2005.06.013.

Abstract

The induction and maintenance of synaptic plasticity is well established to be a Ca2+-dependent process. The use of fluorescent imaging to monitor changes [Ca2+]i in neurones has revealed a diverse array of signaling patterns across the different compartments of the cell. The Ca2+ signals within these compartments are generated by voltage or ligand-gated Ca2+ influx, and release from intracellular stores. The changes in [Ca2+]i are directly linked to the activity of the neurone, thus a neurone's input and output is translated into a dynamic Ca2+ code. Despite considerable progress in measuring this code much still remains to be determined in order to understand how the code is interpreted by the Ca2+ sensors that underlie the induction of compartment-specific plastic changes.

摘要

突触可塑性的诱导和维持是一个依赖Ca2+的过程,这一点已得到充分证实。利用荧光成像监测神经元中[Ca2+]i的变化,揭示了细胞不同区室中各种各样的信号模式。这些区室内的Ca2+信号是由电压门控或配体门控的Ca2+内流以及从细胞内储存库释放产生的。[Ca2+]i的变化与神经元的活动直接相关,因此神经元的输入和输出被转化为动态的Ca2+编码。尽管在测量这种编码方面取得了相当大的进展,但为了理解这种编码是如何被诱导区室特异性可塑性变化的Ca2+传感器解读的,仍有许多问题有待确定。

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