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- W2022286642 abstract "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+." @default.
- W2022286642 created "2016-06-24" @default.
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- W2022286642 date "2002-01-01" @default.
- W2022286642 modified "2023-10-11" @default.
- W2022286642 title "The Life Cycle of Ca2+ Ions in Dendritic Spines" @default.
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- W2022286642 doi "https://doi.org/10.1016/s0896-6273(02)00573-1" @default.
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