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

Voltage-gated Ca(2+) channels activated by action potentials evoke Ca(2+) entry into presynaptic terminals thus briefly distorting the resting Ca(2+) concentration. When this happens, a number of processes are initiated to re-establish the Ca(2+) equilibrium. During the post-spike period, the increased Ca(2+) concentration could enhance the presynaptic Ca(2+) signalling. Some of the mechanisms contributing to presynaptic Ca(2+) dynamics involve endogenous Ca(2+) buffers, Ca(2+) stores, mitochondria, the sodium-calcium exchanger, extraterminal Ca(2+) 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 Ca(2+). Direct evidence for the role of any of these participants in shaping the presynaptic Ca(2+) dynamics comes from direct recordings of giant presynaptic terminals and from fluorescent Ca(2+) imaging of axonal boutons. Here, some of this evidence is presented and discussed.