|  Help  |  About  |  Contact Us

Publication : Evidence for a Clathrin-independent mode of endocytosis at a continuously active sensory synapse.

First Author  Fuchs M Year  2014
Journal  Front Cell Neurosci Volume  8
Pages  60 PubMed ID  24616664
Mgi Jnum  J:250267 Mgi Id  MGI:6099166
Doi  10.3389/fncel.2014.00060 Citation  Fuchs M, et al. (2014) Evidence for a Clathrin-independent mode of endocytosis at a continuously active sensory synapse. Front Cell Neurosci 8:60
abstractText  Synaptic vesicle exocytosis at chemical synapses is followed by compensatory endocytosis. Multiple pathways including Clathrin-mediated retrieval of single vesicles, bulk retrieval of large cisternae, and kiss-and-run retrieval have been reported to contribute to vesicle recycling. Particularly at the continuously active ribbon synapses of retinal photoreceptor and bipolar cells, compensatory endocytosis plays an essential role to provide ongoing vesicle supply. Yet, little is known about the mechanisms that contribute to endocytosis at these highly complex synapses. To identify possible specializations in ribbon synaptic endocytosis during different states of activity, we exposed mice to controlled lighting conditions and compared the distribution of endocytotic proteins at rod and cone photoreceptor, and ON bipolar cell ribbon synapses with light and electron microscopy. In mouse ON bipolar cell terminals, Clathrin-mediated endocytosis seemed to be the dominant mode of endocytosis at all adaptation states analyzed. In contrast, in mouse photoreceptor terminals in addition to Clathrin-coated pits, clusters of membranously connected electron-dense vesicles appeared during prolonged darkness. These clusters labeled for Dynamin3, Endophilin1, and Synaptojanin1, but not for AP180, Clathrin LC, and hsc70. We hypothesize that rod and cone photoreceptors possess an additional Clathrin-independent mode of vesicle retrieval supporting the continuous synaptic vesicle supply during prolonged high activity.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

11 Bio Entities

Trail: Publication

0 Expression