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Victor Matveev

Publications and source records attributed to Victor Matveev.

3 recordsLinked to original sources
PubMed2006

Residual bound Ca2+ can account for the effects of Ca2+ buffers on synaptic facilitation.

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 Ca(2+) influx and proposed that facilitation results from the accumulation of residual Ca(2+) bound to vesicle release triggers. However, this bound Ca(2+) hypothesis appears to contradict the evidence that facilitation is reduced by exogenous Ca(2+) buffers. This conclusion led to a widely held view that facilitation must depend solely on the accumulation of Ca(2+) in free form. Here we consider a more realistic implementation of the bound Ca(2+) mechanism, taking into account spatial diffusion of Ca(2+), and show that a model with slow Ca(2+) unbinding steps can retain sensitivity to free residual Ca(2+). We demonstrate that this model agrees with the facilitation accumulation time course and its biphasic decay exhibited by the crayfish inhibitor neuromuscular junction (NMJ) and relies on fewer assumptions than the most recent variants of the free residual Ca(2+) hypothesis. Further, we show that the bound Ca(2+) accumulation is consistent with Kamiya and Zucker's experimental results, which revealed that photolytic liberation of a fast Ca(2+) buffer decreases the synaptic response within milliseconds. We conclude that Ca(2+) binding processes with slow unbinding times (tens to hundreds of milliseconds) constitute a viable mechanism of synaptic facilitation at some synapses and discuss the experimental evidence for such a mechanism.

Action Potentials↗
PubMed2004

Facilitation through buffer saturation: constraints on endogenous buffering properties.

Synaptic facilitation (SF) is a ubiquitous form of short-term plasticity, regulating synaptic dynamics on fast timescales. Although SF is known to depend on the presynaptic accumulation of Ca(2+), its precise mechanism is still under debate. Recently it has been shown that at certain central synapses SF results at least in part from the progressive saturation of an endogenous Ca(2+) buffer (Blatow et al., 2003), as proposed by Klingauf and Neher (1997). Using computer simulations, we study the magnitude of SF that can be achieved by a buffer saturation mechanism (BSM), and explore its dependence on the endogenous buffering properties. We find that a high SF magnitude can be obtained either by a global saturation of a highly mobile buffer in the entire presynaptic terminal, or a local saturation of a completely immobilized buffer. A characteristic feature of BSM in both cases is that SF magnitude depends nonmonotonically on the buffer concentration. In agreement with results of Blatow et al. (2003), we find that SF grows with increasing distance from the Ca(2+) channel cluster, and increases with increasing external Ca(2+), [Ca(2+)](ext), for small levels of [Ca(2+)](ext). We compare our modeling results with the experimental properties of SF at the crayfish neuromuscular junction, and find that the saturation of an endogenous mobile buffer can explain the observed SF magnitude and its supralinear accumulation time course. However, we show that the BSM predicts slowing of the SF decay rate in the presence of exogenous Ca(2+) buffers, contrary to experimental observations at the crayfish neuromuscular junction. Further modeling and data are required to resolve this aspect of the BSM.

Animals↗