Use-dependent control of presynaptic calcium signalling at central synapses.

Voltage-gated Ca2+ channels activated by action potentials evoke Ca2+ entry into presynaptic terminals thus briefly distorting the resting Ca2+ concentration. When this happens, a number of processes are initiated to re-establish the Ca2+ equilibrium. During the post-spike period, the increased Ca2+ concentration could enhance the presynaptic Ca2+ signalling. Some of the mechanisms contributing to presynaptic Ca2+ dynamics involve endogenous Ca2+ buffers, Ca2+ stores, mitochondria, the sodium–calcium exchanger, extraterminal Ca2+ depletion and presynaptic receptors. Additionally, subthreshold presynaptic depolarization has been proposed to have an effect on release of neurotransmitters through a mechanism involving changes in resting Ca2+. Direct evidence for the role of any of these participants in shaping the presynaptic Ca2+ dynamics comes from direct recordings of giant presynaptic terminals and from fluorescent Ca2+ imaging of axonal boutons. Here, some of this evidence is presented and discussed. [ABSTRACT FROM AUTHOR]