"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
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+.
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]