The life cycle of Ca2+ ions in dendritic spines

被引:538
作者
Sabatini, BL [1 ]
Oertner, TG [1 ]
Svoboda, K [1 ]
机构
[1] Cold Spring Harbor Lab, Howard Hughes Med Inst, Cold Spring Harbor, NY 11724 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S0896-6273(02)00573-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Spine Ca2+ is critical for the induction of synaptic plasticity, but the factors that control Ca2+ handling in dendritic spines under physiological conditions are largely unknown. We studied [Ca2+] signaling in dendritic spines of CA1 pyramidal neurons and find that spines are specialized structures with low endogenous Ca2+ buffer capacity that allows large and extremely rapid [Ca2+] changes. Under physiological conditions, Ca2+ diffusion across the spine neck is negligible, and the spine head functions as a separate compartment on long time scales, allowing localized Ca2+ buildup during trains of synaptic stimuli. Furthermore, the kinetics of Ca2+ sources governs the time course of [Ca2+] signals and may explain the selective activation of long-term synaptic potentiation (LTP) and long-term depression (LTD) by NMDA-R-mediated synaptic Ca2+.
引用
收藏
页码:439 / 452
页数:14
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