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.
Scott
Ricardo
R
Institute of Neurology, Queen Square, London, UK. rscott@ion.ucl.ac.uk
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D006801:Humans; D017136:Ion Transport; D008928:Mitochondria / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000378:metabolism; D017661:Receptors, Presynaptic / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D013569:Synapses / Q000378:metabolism*
D018377:Neurotransmitter Agents; D017661:Receptors, Presynaptic; D019831:Sodium-Calcium Exchanger; D002118:Calcium