Journal
FRONTIERS IN CELLULAR NEUROSCIENCE
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fncel.2015.00239
Keywords
synaptic transmission; synaptic vesicles; short-term plasticity; calcium channels; modeling biological systems
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Funding
- Welcome Trust
- NIH Grant from National Institute for General Medical Sciences [P41 GM103313]
- BBSRC [BB/H011900/1] Funding Source: UKRI
- MRC [MR/M013812/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H011900/1] Funding Source: researchfish
- Medical Research Council [MR/M013812/1] Funding Source: researchfish
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Action potential-dependent release of synaptic vesicles and short-term synaptic plasticity are dynamically regulated by the endogenous Ca2+ buffers that shape [Ca2+] profiles within a presynaptic bouton. Calmodulin is one of the most abundant presynaptic proteins and it binds Ca2+ faster than any other characterized endogenous neuronal Ca2+ buffer. Direct effects of calmodulin on fast presynaptic Ca2+ dynamics and vesicular release however have not been studied in detail. Using experimentally constrained three-dimensional modeling of Ca2+ influx-exocytosis coupling at small excitatory synapses we show that, at physiologically relevant concentrations, Ca2+ buffering by calmodulin plays a dominant role in inhibiting vesicular release and in modulating short-term synaptic plasticity. We also propose a novel and potentially powerful mechanism for short-term facilitation based on Ca2+-dependent dynamic dislocation of calmodulin molecules from the plasma membrane within the active zone.
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