Lecture 2B - Synaptic vesicle cycle transitions between...

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Synaptic vesicle cycle – transitions between transmitter being loaded to vesicles, being mobilized, docking & fusing w/ synaptic membrane, release of NT, reconstitution of vesicle structure, and refilled w/ NT.
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Precursor & enzyme come together to synthesize NTs, which then get pumped into synaptic vesicle. Vesicles get attached to cytoplasmic scaffolding, which waits to be mobilized down to membrane. Vesicles are held to the structure w/ molecule called synapsin. During initial mobilization step b/4 they get down to membrane, there’re some voltage-gated Ca ++ + comes in and binds Ca ++ -calmodulin kinase II ( CAMKII ), which then phosphorylates synapsin and causes it to cleave. Vesicle then is released from scaffolding (made of actin molecule) and migrates down to inner surface of terminal membrane. There’re many steps between mobilization & actual fusion. SNARE hypothesis – hypothesis for how vesicle docks and fuses. SNARE proteins are present on vesicle and also on internal surface of terminal membrane. When vesicle migrates away from reserve pool & gets close to membrane, there’s a SNARE protein on vesicle called synaptic renin and SNARE proteins on membrane called SNAP-25 and syntaxin. As vesicle gets close to membrane, the proteins form a complex that initiates the docking of vesicle. After vesicle’s docked (touching surface of membrane, which is lining w/ voltage-gated Ca ++ channels), there’s a molecule/protein on surface of vesicle called synaptotagmin that acts as a sensor for Ca ++ (figure: black dots of Ca ++ bind on several different spots of synaptotagmin). Synaptotagmin binds Ca ++ , which then causes a change in shape of synaptotagmin molecule (bends & inserts itself into membrane). More Ca ++ binds onto synaptotagmin, which causes further changes in the shape that results in portion of vesicle membrane pulling apart & also pulling on terminal membrane, so that there’s an actual fusion & release of NT into synaptic cleft.
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Synaptotagmin is a Ca ++ sensor & thereby able to trigger/initiate exocytosis (fusion & release) b/c vesicle docks very close to membrane, which is the area of terminal that has highest levels of Ca ++ b/c it has just flow through opened voltage-gated Ca ++ channels. If it happened away from membrane, synaptotagmin might get confused & open at the wrong time. It needs to open right at the internal surface of terminal membrane b/c there’s a very transient high level of Ca ++ right at surface. Endocytosis: once transmitters been released, it reconstitutes vesicle from membrane. Proteins called clathrin binds surface of vesicle membrane, which has been smooched & flattened.
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This note was uploaded on 11/03/2010 for the course BIPN BIPN 142 taught by Professor Wang during the Summer '09 term at UCSD.

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Lecture 2B - Synaptic vesicle cycle transitions between...

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