Ege Kavalali, Ph.D. will present seminar “Quantal neurotransmission and synaptic vesicle recycling” on 10/6/17 from 11-12, LIB110

Ege T. Kavalali Ph.D.,Professor, Rosewood Corporation Chair in Biomedical Science
Department of Neuroscience,U.T. Southwestern Medical Center presenting seminar “Quantal neurotransmission and synaptic vesicle recycling” on 10/6/17, 11-12, LIB 110. Synopsis: Maintenance of synaptic transmission requires constant retrieval and reuse of synaptic vesicles. The executive role of intrasynaptic Ca2+ transients in synaptic vesicle exocytosis is well-established. However, the impact of Ca2+ on synaptic vesicle endocytosis remains unclear. Studies to date paint an extremely complex and seemingly inconsistent picture for the role of Ca2+ in synaptic vesicle endocytosis. However, these observations may not be surprising when compared to our current perspective on Ca2+ regulation of exocytosis. It is now well-established that Ca2+ dependence of exocytosis involves several time scales and multiple Ca2+ sensors where synchronous, asynchronous and spontaneous forms of fusion as well as distinct forms of short term plasticity are all Ca2+-dependent and require on a diverse array of Ca2+ sensors. Therefore, by analogy, it is highly plausible to expect that Ca2+ dependence of endocytosis to be complex and vary in response to distinct stimulation patterns in multiple time scales. This picture is further complicated by parallel operation of multiple synaptic vesicle endocytosis pathways, each with their putatively unique molecular mediators. A major drawback of the studies to date is their reliance on bulk measurements of synaptic vesicle endocytosis, which can be affected by a multitude of factors, such as the number of vesicles involved, the kinetics and duration of Ca2+ signals, as well as accumulation of released substances that may retrogradely alter release and retrieval processes. Therefore, in recent experiments, we aimed to visualize synaptic vesicle exo-endocytosis at the quantal level in order to dissect permissive and instructive signals that regulate synaptic vesicle retrieval. By focusing on single synaptic vesicle trafficking, we could dissociate regulation of release probability from the properties of endocytosis. This work is beginning to specify the exact functions of currently known Ca2+ sensors for endocytosis such as synaptotagmin and potentially identify novel Ca2+ dependent signaling mechanisms that impact synaptic vesicle retrieval and recycling.