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+.
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