Control of Ca2+ influx and calmodulin activation by SK-channels in dendritic spines (dataset)
Griffith, Thom; Tsaneva-Atanasova, Krasimira; Mellor, Jack
Date: 5 May 2016
Dataset
Publisher
University of Exeter
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Abstract
The key trigger for Hebbian synaptic plasticity is influx of Ca2+ into postsynaptic
dendritic spines. The magnitude of [Ca2+] increase caused by NMDA-receptor
(NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought to determine
both the amplitude and direction of synaptic plasticity by differential activation of ...
The key trigger for Hebbian synaptic plasticity is influx of Ca2+ into postsynaptic
dendritic spines. The magnitude of [Ca2+] increase caused by NMDA-receptor
(NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought to determine
both the amplitude and direction of synaptic plasticity by differential activation of Ca2+
-sensitive enzymes such as calmodulin. Ca2+ influx is negatively regulated by Ca2+
-activated K+ channels (SK-channels) which are in turn inhibited by neuromodulators
such as acetylcholine. However, the precise mechanisms by which SK-channels control
the induction of synaptic plasticity remain unclear. Using a 3-dimensional model of
Ca2+ and calmodulin dynamics within an idealised, but biophysically-plausible,
dendritic spine, we show that SK-channels regulate calmodulin activation specifically
during neuron-firing patterns associated with induction of spike timing-dependent
plasticity. SK-channel activation and the subsequent reduction in Ca2+ influx through
NMDARs and L-type VGCCs results in an order of magnitude decrease in calmodulin (CaM)
activation, providing a mechanism for the effective gating of synaptic plasticity
induction. This provides a common mechanism for the regulation of synaptic plasticity
by neuromodulators.
Mathematics and Statistics
Faculty of Environment, Science and Economy
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