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The life cycle of Ca(2+) ions in dendritic spines.

Abstract：

:Spine Ca(2+) is critical for the induction of synaptic plasticity, but the factors that control Ca(2+) handling in dendritic spines under physiological conditions are largely unknown. We studied [Ca(2+)] signaling in dendritic spines of CA1 pyramidal neurons and find that spines are specialized structures with low endogenous Ca(2+) buffer capacity that allows large and extremely rapid [Ca(2+)] changes. Under physiological conditions, Ca(2+) diffusion across the spine neck is negligible, and the spine head functions as a separate compartment on long time scales, allowing localized Ca(2+) buildup during trains of synaptic stimuli. Furthermore, the kinetics of Ca(2+) sources governs the time course of [Ca(2+)] signals and may explain the selective activation of long-term synaptic potentiation (LTP) and long-term depression (LTD) by NMDA-R-mediated synaptic Ca(2+).

journal_name

Neuron

journal_title

Neuron

authors

Sabatini BL,Oertner TG,Svoboda K

doi

10.1016/s0896-6273(02)00573-1

subject

Has Abstract

pub_date

2002-01-31 00:00:00

pages

439-52

issue

3

eissn

0896-6273

issn

1097-4199

pii

S0896627302005731

journal_volume

33

pub_type

杂志文章

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