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Neuropsychopharmacology > Lecture 4 > Flashcards

Lecture 4 Flashcards

(75 cards)

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1
Q

what is the process of environmental toxicology?

A

seeing the effects of a chemical on 1. the environment 2. other organisms 3. food chain 4. organisms up/down the food chain

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2
Q

what is the process of pharmacokinetics & pharmacodynamics?

A

seeing how a chemical affects 1. the patient 2. intended target tissues and potential therapeutic effects 3. unintended targets 4. toxic effects

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3
Q

colloquial definition of pharmacokinetics

A

what the body does to the drug
- how the body responds to get rid of it

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4
Q

colloquial definition of pharmacodynamics

A

what the drug does to the body
- effect in your CNS

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5
Q

speed of neuropeptide transmission

A

slow

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6
Q

speed of SM NT neurotransmission

A

fast

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7
Q

why is there a difference in speed of neurotranmission b/w SM and neuropeptides

A

primary receptor target location

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8
Q

characteristics of SM NT effects

A

most have instantaneous effect

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9
Q

characteristics of NP NTs effects

A

different receptors & longer effects

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10
Q

ligand-gated ion channels location

A

membrane

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11
Q

ligand-gated ion channels effector

A

channel

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12
Q

ligand-gated ion channels coupling

A

direct

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13
Q

ligand-gated ion channels examples

A

nicotinic receptor, GABAAR

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14
Q

ligand-gated ion channels time scale

A

milliseconds

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15
Q

GPCR location

A

membrane

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16
Q

GPCR effector

A

channel or enzyme

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17
Q

GPCR coupling

A

G protein

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18
Q

GPCR examples

A

muscarinic receptor, adrenoreceptors

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19
Q

GPCR time scale for cellular effects

A

seconds

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20
Q

structure of GPCR

A

transmembrane-spanning receptor w/ a N terminus outside the cell & C terminus inside

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21
Q

what structural change occurs when GPCRs are activated

A

3D change that allows it to couple G protein, leading to other downstream changes

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22
Q

which is faster; ligand-gated or GPCR

A

ligand-gated, bc GPCR requires so many bindings and changes

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23
Q

two types of ion channels

A

voltage-gated & ligand-gated

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24
Q

requirement for voltage-gated channel to activate

A

membrane potential change

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25
ionotropic receptor activation requirement
binding of NTs to the channel
26
ionotropic channel structure
- formed of subunits
27
metabotropic function
activates a G protein (trimeric protein w/ alpha, beta, gamma subunits)
28
function of metabotropic C terminus
dictates which 2nd messenger system is activated
29
how do metabotropic channels mediate voltage-gated channels
less directly by the generation of diffusible 2nd messengers
30
what does the alpha G protein subunit do
either inhibits or excites adenyl cyclase, which changes cAMP levels, which changes transcriptional factors
31
what does the beta-gamma subunit do
modulates ion channels
32
biased agonism
multiple drugs can bind a single receptor, but they may activate different sets of 2nd messenger systems w/ different downstream effects
33
significance of G alpha subunit in opioid receptors
involves engagement of MAP kinase pathways, and is associated w/ respiratory depression of opioids
34
endogenous ligand
the molecule your brain produces
35
places for binding
orthosteric site, allosteric site
36
orthosteric site
where the endogenous ligand binds to the receptor
37
allosteric site
a different site than the endogenous ligand binding
38
natural ligand binding effect
causes receptor activation
39
agonist binding effect
full drug effect; causes receptor activation
40
partial agonist binding effect
only causes a partial effect, w/ some activation but not maximum effect
41
antagonist binding effect
preventing drug effect - does not cause activation & prevents the natural ligand from binding
42
inverse agonist binding effect
opposite effect of what natural ligand is doing; eg binds same site but activates instead of inhibiting
43
characteristics of Buprenorphine as a partial agonist
high receptor binding affinity, but doesn't cause the conformational change to cause the same downstream effects as fentanyl - difficult to get respiratory depression unless you take a ton
44
how is binding measured
by total # of available receptors - usually determined w/ radioactive drug molecules
45
how is binding affinity related to effect size
not necessarily related
46
what can you measure by determining receptor activation
measure of response
47
what is the significance of spare receptors to receptor activation
you can have maximal effect w/o activating all available receptors
48
what is Kd
equilibrium dissociation constant; represents concentrations required to occupy 50% of the receptor binding sites at equilibrium (aka # of receptors bound at 50%)
49
what does lower Kd mean
stronger receptor binding (higher affinity for receptor) & lower drug concentration needed to produce binding
50
ED50
effective dose that produces 50% of maximal response
51
what is potency
concentration (EC50) or dose (ED50) of a drug required to produce 50% of drug's maximal effect
52
what is efficiency (Emax)
maximum effect that can be expected from the drug
53
what happens if you increase the dose after you reach Emax
does not produce a greater magnitude of effect
54
how do agonists produce their effects
drugs occupy receptors & activate them
55
how do antagonists produce their effects
occupy receptors but do not activate them - block agonist activity
56
do allosteric sites usually independently activate a receptor?
no, usually require the endogenous ligand to also be there - can be inhibiting or activating
57
what is a competitive antagonist
competes for the same binding site w/ an agonist & binding is mutually exclusive
58
how does competitive antagonist binding affect potency & efficacy
shift in potency, slight shift in efficacy
59
noncompetitive antagonist function
can prevent the action of an agonist w/o any effect on the binding of the agonist to the receptor
60
how can a cell overcome a competitive agonist
by flooding with endogenous ligand
61
how can a cell overcome noncompetitive antagonists
by adding more receptors
62
are you able to get the maximum effect when bound by a noncompetitive antagonist?
no
63
how is potency & efficacy affected by noncompetitive antagonists
always reduction in efficacy & shift in potency
64
what is drug chirality/stereochemistry
the spatial arrangement of atoms within a drug molecule that gives rise to different enantiomers
65
what are enantiomers
mirror images of each other that cannot be superimposed
66
why does chirality matter to biological activity
one enantiomer may be therapeutically active while the other is inactive or harmful
67
why is thalidomide significant to chirality
was used as an antinausea drug but the enantiomer had birth defective effects
68
why does chirality matter to receptor specificity
many biological targets (like enzymes & receptors) are chiral themselves, so one enantiomer might fit well while the other does not
69
significance of ibuprofen to chirality
only S-enantiomer is active as pain reliever
70
why does chirality matter for metabolism & safety
body may metabolize each enantiomer differently, leading to variations in efficacy & side effects
71
significance of Methadone to chirality
R-enantiomer is more potent as an opioid agonist than S-enantiomer
72
racemic mixture
contains equal amounts of both enantiomers
73
what questions are answered during animal testing
how long does it stay in the body? does it harm other organs?
74
how long does protection for your drug last
from the time you file the patent to the end of the clinical trials
75

Neuropsychopharmacology (8 decks)

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