dc.contributor.author | Griffith, Thom | |
dc.contributor.author | Tsaneva-Atanasova, Krasimira | |
dc.contributor.author | Mellor, Jack | |
dc.date.accessioned | 2016-05-05T14:12:37Z | |
dc.date.issued | 2016-05-05 | |
dc.description.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. | en_GB |
dc.identifier.uri | http://hdl.handle.net/10871/21394 | |
dc.language.iso | en | en_GB |
dc.publisher | University of Exeter | en_GB |
dc.relation.url | http://hdl.handle.net/10871/21745 | en_GB |
dc.title | Control of Ca2+ influx and calmodulin activation by SK-channels in dendritic spines (dataset) | en_GB |
dc.type | Dataset | en_GB |
dc.date.available | 2016-05-05T14:12:37Z | |
dc.description | A 3-dimensional model of Ca2+ and calmodulin dynamics within an idealised, but biophysically-plausible,
dendritic spine, demonstrates that SK-channels regulate calmodulin activation specifically during neurone firing patterns associated with induction of spike timing-dependent plasticity. | en_GB |
dc.description | The journal article associated with this dataset is available at: http://hdl.handle.net/10871/21745. | en_GB |
dc.identifier.journal | PLoS Computational Biology | en_GB |