| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4351503 | Neuroscience Research | 2012 | 7 Pages |
Action potentials, when arriving at presynaptic terminals, elicit Ca2+ influx through voltage-gated Ca2+ channels. Intracellular [Ca2+] elevation around the channels subsequently triggers synaptic vesicle exocytosis and also induces various protein reactions that regulate vesicle endocytosis and recycling to provide for long-term sustainability of synaptic transmission. Recent studies using membrane capacitance measurements, as well as high-resolution optical imaging, have revealed that the dominant type of synaptic vesicle endocytosis at central nervous system synapses is mediated by clathrin and dynamin. Furthermore, Ca2+-dependent mechanisms regulating endocytosis may operate in different ways depending on the distance from Ca2+ channels: (1) intracellular Ca2+ in the immediate vicinity of a Ca2+ channel plays an essential role in triggering endocytosis, and (2) intracellular Ca2+ traveling far from the channels has a modulatory effect on endocytosis at the periactive zone. Here, I integrate the latest progress in this field to propose a compartmental model for regulation of vesicle endocytosis at synapses and discuss the possible roles of presynaptic Ca2+-binding proteins including calmodulin, calcineurin and synaptotagmin.
► The current state of knowledge on synaptic vesicle endocytosis is described. ► A novel compartmental model for the role of Ca2+ in vesicle endocytosis is proposed. ► The possible roles of Ca2+-sensing proteins in vesicle endocytosis are discussed.
