Ca2+ and synaptic plasticity

被引:63
作者
Cavazzini, M
Bliss, T
Emptage, N
机构
[1] Natl Inst Med Res, Div Neurophysiol, London NW7 1AA, England
[2] Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England
基金
英国医学研究理事会;
关键词
calcium; hippocampus; receptors; N-methyl-D-aspartate; voltage-gated channels; synapses; dendrites; long-term depression; long-term potentiation; neuronal plasticity; endoplasmic reticulum; calcium signaling; inositol 1,4,5-trisphosphate; ryanodine;
D O I
10.1016/j.ceca.2005.06.013
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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. (C) 2005 Published by Elsevier Ltd.
引用
收藏
页码:355 / 367
页数:13
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