Regulation of Endocytosis at Mammalian Central Synapses

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dc.contributor.advisorWu, Ling-Gangen_US
dc.contributor.advisorPick, Leslieen_US
dc.contributor.authorShi, Boen_US
dc.contributor.departmentBiologyen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.date.accessioned2022-06-21T05:32:36Z
dc.date.available2022-06-21T05:32:36Z
dc.date.issued2022en_US
dc.description.abstractSynaptic endocytosis retrieves exocytosed vesicles and maintains synaptic transmission which is essential to neural circuit functions. Accumulated studies suggest that calcium influx triggers synaptic vesicle endocytosis, which must undergo membrane pit formation and fission of the pit’s neck to generate vesicles. However, the calcium sensor that links calcium to endocytic machinery remains not well understood; whether pit formation involves clathrin remains debated, what mechanism controls the endocytic vesicle size remains not well understood either; the mechanism that couples exo- to endocytosis remains not fully understood either. My thesis work aims at improving our understanding of each of these questions. I studied endocytosis using a combination of techniques, including gene knockout, gene knockdown, fluorescence imaging, electron microscopy, and molecular biology techniques. I identified the calcium sensors that link calcium influx to endocytosis – the protein kinase C α and β isoforms and calmodulin. I found that clathrin is involved in mediating endocytosis at synapses, which may clarify the doubts on whether clathrin is indispensable for synaptic vesicle endocytosis. I found that dynamin is crucial not only for fission as generally thought, but also for controlling the vesicle size at hippocampal synapses, which enhances our understanding on how vesicle size is regulated at synapses. I found that NSF, which disassembles the SNARE complex, is crucial for mediating synaptic vesicle endocytosis, which enhance our understanding of the mechanisms that couple exo- to endocytosis. Consequently, In summary, I identified endocytosis calcium sensor as protein kinase C (α and β isoforms) and calmodulin; found clathrin in playing a role in pit formation, discovered a novel function of dynamin in controlling vesicle size, and reveal NSF in coupling exo- to endocytosis. These findings contribute to better understanding regulation of endocytosis at synapses.en_US
dc.identifierhttps://doi.org/10.13016/oztd-fqty
dc.identifier.urihttp://hdl.handle.net/1903/28906
dc.language.isoenen_US
dc.subject.pqcontrolledBiologyen_US
dc.subject.pqcontrolledNeurosciencesen_US
dc.subject.pquncontrolledcalmodulinen_US
dc.subject.pquncontrolledclathrinen_US
dc.subject.pquncontrolleddynaminen_US
dc.subject.pquncontrolledendocytosisen_US
dc.subject.pquncontrolledNSFen_US
dc.subject.pquncontrolledPKCen_US
dc.titleRegulation of Endocytosis at Mammalian Central Synapsesen_US
dc.typeDissertationen_US

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