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direct
binds to / interferes with where the NTs bind to receptor
indirect
does not interfere with NT binding site
agonist
facilitate or help the postsynaptic effect
antagonist
impairs or hurts the postsynaptic effects
PCP binding site
where phencyclidine (PCP) binds
PCP is a…
indirect antagonist
GABA receptor binding sites
there are GABA ionotropic and metabotropic channels for different things (Cl- ionotropic, K+ metabotropic) → both inhibitory
alcohol seems to bind to benzodrazepene site
barbituates are sedative → direct agonist
picrotoxin → direct antagonist
if antagonist inhibitory → it’s excitatory
drug effects pre-synapse
drug serves as precursor
drug inactivates synthetic enzyme; inhibits synthesis of NT ANT
drug prevents storage of NT in vesicles ANT
drug stimulates release of NT AGO
drug inhibits release of NT ANT
drug stimulates postsynaptic receptors AGO
drug blocks postsynaptic receptors ANT
drug stimulates autoreceptors; inhibits synthesis/release of NT ANT
drug blocks autoreceptors, increase synthesis/release of NT AGO
drug blocks reuptake AGO
drug inactivates acetychloinestarase AGO
selective serotonin reuptake inhibitors (SSRIs)
inhibit reuptake → leave serotonin in cleft → more opportunity for serotonin to bind (more serotonin in cleft, more to bind to)
developed in 1970s based on serotonin hypothesis of depression
technically have presynaptic effects but culminate to have postsynaptic effects