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blue = lecture

green = reading

yellow = article

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most are chemical

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ligand-gated ion channels vs G-protein-coupled receptors (GPCRs)

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ligand-gated ion channels vs G-protein-coupled receptors (GPCRs)

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ionotropic = ligand gated

type of metabotropic channel = GPCR

when NT is released, communicated w receptors on the post-synaptic side to effect a response

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if receptor is ligand gated, ions flow through channel to change membrane potential of post synaptic cell

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relationship between synaptic vesicle exocytosis and quantal transmitter release

1 quanta of NT = 1 vesicle fusing

Katz looked at the NMJ = end plates

EPP: end plate potential

change in membrane potential such that an AP of the presynpatic neurons can elicit a depolarization of the muscle fibers

summation of many quanta release

mEPPs - mini

spontaneous release

1 quanta of NT, discrete packet of

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synaptic vesicles (SV)

generated from any of the endosomes in the endosomal pathway

generated in the soma then trafficked to the axon terminal

secretory granules (SG) = dense core vesicles bc it's electron dense

generated form the Golgi initially as immature secretory granules then mature into secretory granules

generated in Golgi of the soma then trafficked to the axon terminal

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release of NT at the active zone of a synapse

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release of NT at the active zone of a synapse

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vesicles have proteins attached to them

proteins tell the vesicle where its going to help it fuse w its target membrane

VGLUT --> this is a glutamate vesicle --> carried glutamate NT

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vesicles are made of phospholipids

must overcome hydrophilic heads repulsion, so force must be applied

SNARE complex generates the force necessary to fuse plasma and vesicle membrane to allow exocytosis

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has

SNAP-25 (a t-SNARE)

Syntaxin (a t-SNARE)

together: SNAP-25, syntaxin, and synaptobrevin make up the SNARE complex

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kiss and run: vesicle targets, tethers, and docks like all other vesicles; during exocyotosis, vesicle membrane DOESN'T fully fuse w the plasma membrane, only opens to release contents, then reseals

full fusion: normal vesicle target, tether, and dock; vesicle fully fuses w plasma membrane

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clathrin mediated endocytosis, after full fusion

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clathrin mediated endocytosis, after full fusion

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goal: tight correspondence btwn neuronal activity and synchronous releases of NTs

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goal: tight correspondence btwn neuronal activity and synchronous releases of NTs

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synaptic vesicles are releases from the active zone: a stretch of synaptic membrane facing the postsynaptic vesicle across the divide of the synaptic cleft

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some synaptic vesicles are docked at the active zone then primed for release by protein complexes that bring them into extreme proximity of the plasma membrane

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NTs molecules passively diffuse across the synaptic cleft to reach the post synaptic cell

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active zone membrane is endocytosed and synaptic vesicles membrane proteins are then reassembled into recycled synaptic vesicles --> used for more NT releases

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minimize spontaneous release

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synchronous release to neuronal activity

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protein complex at the active zone that docks some synaptic vesicles to the active zone

synaptic vesicles are primed for triggered release by conformational changes in SNAREpin and simultaneously prevented from spontaneous release through interactions btwn complexin and SNAREpin

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end plate is the current at the end of post synaptic side of the NMJ in an intact organism

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vesicle is different if the NTs are small molecule or peptide NTs

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V-SNARE, VAMP, or synaptobrevin

a neurotransmitter (loads the NT vesicles)

synaptotagmin (the Ca sensor)

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need recycling bc there would be too many vesicles on the synapses and there wouldn't be space for more vesicles

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SNARE complex:

vSNARE = VAMP = synaptobrevin (in red in the picture)

SNAREpin (in blue in the picture)

SNAP-25

synatxin

synaptotagnin: senses change in [Ca], allows release of complexin

complexin: allows SNARE complex to change from trans to cis conformation --> exocytosis

when there isn't an action potential occurring, vesicles are being held at the presynaptic membrane in the SNARE protein. complexin inhibits conformation of SNARE complex that would allow exocytosis. when syntaxin detects change in [Ca] during action potential, it allows complexin to release, so the SNARE complex zip together (picture), allowing exocytosis of NTs in the vesicle

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psilocybin might be effective for mood disorder and substance use disorders

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reduced amygdala response to negative affect stimuli

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!!! in all brain regions, BOLD change returned to baseline after 1 month, only negative after 1 week

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!!! in all brain regions, BOLD change returned to baseline after 1 month, only negative after 1 week

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increased number of significant resting-state functional connection from baseline --> 1 week --> 1 month

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mostly created prefrontal and temporal functional connections during all durations of treatment

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mostly created prefrontal and temporal functional connections during all durations of treatment

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psilocybin might not be as effective after 1 month bc of psilocybin's half life, but change observed after 1 week might be bc psilocybin improves top-down processing to pt's can have more brain region regulation in response to emotional stimuli

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reported in other lit: increase in amygdala activity 1 day after treatment

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reported in other lit: increase in amygdala activity 1 day after treatment

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increase in amygdala response to emotional stimuli 1 day after psilocybin treatment might be due to serotonergic adaptation (5 HT receptors) to treatment, that this study demonstrates is stabilized after 1 week