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resting membrane potential- where is sodium and potassium. how many come in and out?
sodium- more outside than inside
potassium- more inside the outside
allows it to do work when gates open- changes polarity
3 sodium in and 2 potassium
what influences if an ion will move
chemical- ions will tend to flow down
electrical gradient- if negative inside ions will flow down
permeability of membrane
na/k atpase
what is an action potential briefly
excitation stimulus- will allow sodium ions to flow into cell
how do ligand gates work? does this cause A.P?
signal binds to ligand- changes confirmation and it opens- sodium
channel opens and flow through difussion- inside becomes very POSITIVE- sodium
inside becomes DEPOLARISED
voltage moves towards neutral- more is needed for action potential though- -55mV
what are the triggers for depolarisation and neurotransmitter release?
Na is the ELECRICAL- as it changes the voltage- allows Ca2+ voltage channels to open
Ca2+ is the CHEMICAL for NT. release- changes biochemistry in vesicle
what is the synaptic vesicle cycle steps?
active filling of vesicles
clustering in active zone
docking of these at active zone- attach to Ca2+ channels
priming with SNARE complexes
calcium triggering fusion
recycling
key proteins for neurotransmitter release?
VAMPs- v-SNAREs
syntaxin- t-SNARE
synaptotagmin- Calcium CENSOR- binds to C2A and C2B and raises affinity for calcium.
ALL HAVE ALPHA HELICES- pull vesicle down to cell membrane
neurotransmitter release steps
sodium gates open- Na
cause depolarisation within cell- opens voltage depend Calcium channels
calcium flows in
synaptotgamin in the active zone bind to calcium
causes exocytosis- fusion of vesicles to membrane using SNARE complexes
models of recycling
kiss and run- vesicles don’t fully fuse- very quick
Clathrin mediated endocytosis- fuse with membrane and new vesicle is made with Clathrin
ultrafast endocytosis budding- new vesicle made end-some