Format

Send to

Choose Destination
Neurosci Res. 2012 May;73(1):1-7. doi: 10.1016/j.neures.2012.02.012. Epub 2012 Mar 3.

Ca2+-dependent regulation of synaptic vesicle endocytosis.

Author information

1
Brain Mind Institute, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland. takayuki.yamashita@epfl.ch

Abstract

Action potentials, when arriving at presynaptic terminals, elicit Ca(2+) influx through voltage-gated Ca(2+) channels. Intracellular [Ca(2+)] 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, Ca(2+)-dependent mechanisms regulating endocytosis may operate in different ways depending on the distance from Ca(2+) channels: (1) intracellular Ca(2+) in the immediate vicinity of a Ca(2+) channel plays an essential role in triggering endocytosis, and (2) intracellular Ca(2+) 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 Ca(2+)-binding proteins including calmodulin, calcineurin and synaptotagmin.

PMID:
22401840
DOI:
10.1016/j.neures.2012.02.012
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center