CRM: Centro De Giorgi
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Nanoscale mathematical modeling of synaptic transmission, calcium dynamics, transduction and cell sensing

course: Modelling of Ca2+ influx and calmodulin activation in dendritic spines: implications for synaptic plasticity

speaker: Krasimira Tsaneva-Atanasova (University of Exeter)

abstract: It is an open question how the multiple special and temporal scales involved in intracellular Ca2+ handling as part of Spike-Timing-Dependent Plasticity models affect the plasticity outcomes predicted by these models. Hebbian or associative plasticity is triggered by postsynaptic Ca2+ influx which activates calmodulin and CaMKII. The influx of Ca2+ through voltage-dependent NMDA receptors and Ca2+ channels is regulated by Ca2+ -activated K+ channels (SK-channels) providing negative feedback regulation of postsynaptic Ca2+. Using 3-dimensional spatio-temporal modelling of Ca2+ and calmodulin dynamics within dendritic spines we show that the non-linear relationship between Ca2+ influx and calmodulin activation endows SK-channels with the ability to “gate” calmodulin activation and therefore the induction of Hebbian synaptic plasticity. Since SK-channels are inhibited by several neuro-modulator receptors including acetylcholine and noradrenaline, the gating of synaptic plasticity by SK-channels could represent a common mechanism by which neuro-modulators control the induction of synaptic plasticity.

Mon 8 Oct, 9:30 - 10:30, Aula Dini
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