Paper Info
Title
Control of Ca2+ Influx and Calmodulin Activation by SK-Channels in Dendritic Spines.
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 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.
Year
DOI
Venue
2016
10.1371/journal.pcbi.1004949
PLOS COMPUTATIONAL BIOLOGY
Field
DocType
Volume
Synaptic scaling,Nonsynaptic plasticity,Anatomy,Biology,Biophysics,Synaptic augmentation,Synaptic plasticity,Genetics,Metaplasticity,Synaptic fatigue,SK channel,Homosynaptic plasticity
Journal
12
Issue
ISSN
Citations 
5
1553-7358
0
PageRank 
References 
Authors
0.34
2
3
Name
Order
Citations
PageRank
Thom Griffith100.34
Krasimira Tsaneva-Atanasova203.04
Jack R Mellor300.34