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

"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+. ..."

Model Type: Molecular Network

Model Concept(s): Facilitation; Calcium dynamics

Simulation Environment: CalC Calcium Calculator (web link to model)


Matveev V, Bertram R, Sherman A. (2006). Residual bound Ca2+ can account for the effects of Ca2+ buffers on synaptic facilitation. Journal of neurophysiology. 96 [PubMed]

This website requires cookies and limited processing of your personal data in order to function. By continuing to browse or otherwise use this site, you are agreeing to this use. See our Privacy policy and how to cite and terms of use.