Facilitation model based on bound Ca2+ (Matveev et al. 2006)

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"Facilitation is a transient stimulation-induced increase in synaptic response, a ubiquitous form of short-term synaptic plasticity that can regulate synaptic transmission on fast time scales. In their pioneering work, Katz and Miledi and Rahamimoff demonstrated the dependence of facilitation on presynaptic Ca2+ influx and proposed that facilitation results from the accumulation of residual Ca2+ bound to vesicle release triggers. However, this bound Ca2+ hypothesis appears to contradict the evidence that facilitation is reduced by exogenous Ca2+ buffers. This conclusion led to a widely held view that facilitation must depend solely on the accumulation of Ca2+ in free form. Here we consider a more realistic implementation of the bound Ca2+ mechanism, taking into account spatial diffusion of Ca2+, and show that a model with slow Ca2+ unbinding steps can retain sensitivity to free residual Ca2+. ..."
1 . Matveev V, Bertram R, Sherman A (2006) Residual bound Ca2+ can account for the effects of Ca2+ buffers on synaptic facilitation. J Neurophysiol 96:3389-97 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Molecular Network;
Brain Region(s)/Organism:
Cell Type(s):
Gap Junctions:
Simulation Environment: CalC Calcium Calculator (web link to model);
Model Concept(s): Facilitation; Calcium dynamics;
(located via links below)
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