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• W2100060186 abstract "Synaptic plasticity is induced by the influx of calcium ions (Ca2+) through N-methyl-D-aspartate receptors (NMDARs), and the direction and strength of the response depend on the frequency of the synaptic inputs. Recent studies have shown that the direction of synaptic plasticity is also governed by two distinct NMDAR subtypes (NR1/NR2A, NR1/NR2B). How are the different types of regulation (frequency-dependent and receptor-specific) processed simultaneously? To clarify the molecular basis of this dual dependence of synaptic plasticity, we have developed a mathematical model of spatial Ca2+ signaling in a dendritic spine. Our simulations revealed that calmodulin (CaM) activation in the vicinity of NMDARs is strongly affected by the diffusion coefficient of CaM itself, and that this 'local CaM diffusion system' works as a dual decoder of both the frequency of Ca2+ influxes and their postsynaptic current shapes, generated by two NMDAR subtypes, implying that spatial factors may underlie the complicated regulation scheme of synaptic plasticity." @default.
• W2100060186 created "2016-06-24" @default.
• W2100060186 creator A5003925893 @default.
• W2100060186 creator A5072540019 @default.
• W2100060186 creator A5082949989 @default.
• W2100060186 date "2005-01-01" @default.
• W2100060186 modified "2023-10-15" @default.
• W2100060186 title "Local signaling with molecular diffusion as a decoder of Ca ²⁺ signals in synaptic plasticity" @default.
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• W2100060186 doi "https://doi.org/10.1038/msb4100035" @default.
• W2100060186 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1681445" @default.
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