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Psychopharmacology > Exam 1: Dynamics > Flashcards

Exam 1: Dynamics Flashcards

1
Q

Pharmacodynamics

A

study of physiological and biochemical interaction of drug molecules with target tissue that is responsible for ultimate effects of drug

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2
Q

Large protein molecules located on cell surface/within cells that are initial sites of action of biological active agents

A

receptor

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3
Q

Two types of receptors

A

cell surface-extracellular

Intracellular: cytoplasm/nucleus

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4
Q

Most hormones that acat on brain to influence neural events use ___ receptor

A

intracellular

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5
Q

high affinity

A

attach most readily

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6
Q

low effiacy

A

can attach, but doesn’t do anything

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7
Q

antagonist

A

block effect

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8
Q

agonist

A

act as NT

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9
Q

Partial agonists

A

efficacy less than full agonists, but more than antagonist

-effect, but not as much

Technically some intrinsic activity

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10
Q

Inverse agonists

A

initiate biological action, but action is opposite to agonist

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11
Q

Receptor number modification

A

long term regulation:

up-regulation: increase receptors

down regulation: decrease receptors

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12
Q

Receptors modified in sensitivity

A

more rapid regulation via 2nd messengers

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13
Q

The idea that receptor proteins have different characteristics in different target tissue

A

receptor subtypes

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14
Q

Does response curve

A

describes the extent of biological/behavioral effect (mean response in population) produced by given [drug]

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15
Q

ED50

A

dose that produces 1/2 maximal effect

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16
Q

ED100

A

maximum response occurs at does which we assume receptors fully occupied

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17
Q

Potency

A

absolute amount of drug necessary to produce a specific effect

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18
Q

maximum on y-axis

A

efficacy

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19
Q

TD50

A

does at which 50% of the population experiences a particular toxic effect

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20
Q

Therapeutic index

A

TI= TD50 / ED50

LD50 / ED 50

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21
Q

Factor index

A

dose of drug that is lethal to 1% of the population compared with the dose that is therapeutically effective in 99% of the population (LD1 / ED99)

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22
Q

Competitive Antagonists

A

can be displaced from sites by excess of agonist because increase [drug] competes more effectively for fixed receptors

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23
Q

Noncompetitive antagonists

A

drugs that reduce effects of agonists in ways other than competing for the receptor.

e.i. binding to portion of receptor other than agonist binding site

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24
Q

Physiological antagonism

A

two drugs that act in 2 distinct ways but interact in such a way that they reduce each other’s effectiveness in the body

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25
Q

Potentiation

A

situation in which combo of 2 drugs produces effects that are greater than the sum of their individual effects.

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26
Q

Radioligand binding

A

used to study number of receptors in given region

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27
Q

Radioligand: to measure amount of ligand that binds to sites we are concerned with, add

A

very high [nonradioactive competing ligand] to some tubes to show most radioactive binding displaced.

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28
Q

radioligand: ___ binding subtracted when data for specific binding calculated

A

nonspecific

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29
Q

Saturability

A

finite # receptors in tissue.

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30
Q

Point at which binding curve plateus

A

Bmax

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31
Q

If you compare rate of dissociation with rate of binding, you get ___

A

Kd

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32
Q

Kd

A

dissociation constant, measure of drug affinity for specific receptor

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33
Q

Autoradiogarphy

A

use radio ligand on slides instead of ground up tissue

shows radio bound ligand and its location, good fro studying effects of brain lesions.

34
Q

In vivo receptor binding

A

shows researcher where particular drug/NT binds in intact animal

35
Q

Dose response curves only show

A

POTENCY

36
Q

Increase potency

A

decrease ED50 (EC50?)

37
Q

Increase potency

A

lower x-axis value

38
Q

Increase efficacy

A

increase Bmax

39
Q

Factors determining drug potency

A

1) Accessibility (kinetics)
2) affinity (dynamics)
3) intrinsic activity (dynamics)

40
Q

affinity

A

drug binds to receptors

quantitative measure of attraction between drug molecules and receptors

41
Q

intrinsic activity

A

cellular response

42
Q

k1

A

D + R –> DR

Rate at which drug ASSOCIATES with receptor

43
Q

k2

A

DR –> D + R

Rate at which drug DISSOCIATES from receptor

44
Q

how do you measure drug affinity?

A

3H radio ligand label

Substitute 3H (tritium) in for hydrogen

Tritium= PNN

45
Q

QNB

A

binds to acetylcholine mucurinic receptors

46
Q

Beta particle emission: radio isotope

A

Tritium PNN unstable, so decays to helium-3 PPN

47
Q

Radioligand receptor binding is…

A

transient, reversible, selective

saturable, displacement

48
Q

increase affinity:
k1 ___
k2 ___

A

k1 fast

k2 slow

49
Q

kd =

A

k2/k1

50
Q

kd (dissociation), how do we determine?

A

saturation experiment

[radioligand] that labeled 50% receptor in sample

51
Q

Ki (inhibition constant), how do we determine?

A

Competition experiment, [drug] that displaces 50% of radio ligand bound in sample

52
Q

Affinity of drug for receptor

A

Kd

53
Q

total number of receptors

A

Bmax

54
Q

Saturation experiment

A

3H ligand
tissue prep
incubation for 1 hour
total binding = Specific binding (SB) +NSB (bound to membrane)

T= total binding 
SB = T - NSB

Y-axis: SRB
x-axis: [radioligand]

55
Q

Increase affinity means ____ Kd

A

lower Kd

56
Q

Competition experiment: radioactive form of drug not available

A

allows direct comparison of affinities of several different drugs

Same as saturation, but now varied amounts of competitor ligand too

y-axis: % SB of RL
x-axis: log [competitor] M

57
Q

increasing affinity

A

decrease KI

58
Q

Intrinsic Activity:

A

activation of cellular activity by drug

59
Q

Agonist

A

increase affinity, mimic NT (similar cell response)

fully/partially stimulate receptors (intrinsic activity)

60
Q

Antagonist

A

Increase affinity, block receptors (no NT response)
no intrinsic activity, don’t stimulate receptors

NO INTRINSIC ACTIVITY

61
Q

Affinity

A

molecular attraction between drug and receptor

62
Q

Intrinsic Activity

A

Activation of Cellular activity by drug

63
Q

Partial + Full agonist

A

weaker than if just full

64
Q

Primary site of drug action

A

synapse

65
Q

3 Ways to remove a transmitter

A

1) Enzymes
2) Reuptake
3) Glial Reuptake

66
Q

Ionotropic Receptors

A

Fast synaptic transmission (ms)
Subunits around central ion
ions go through

67
Q

Ionotropic examples

A

acetylcholine
GABA-A
5-HT3

68
Q

Metabotropic

A

cell surface receptors regulate activity

Slower (s)
peptides
alpha/beta subunits activate effectors

Agonist receptor bind > Gprotein dissociation

PHOSPHORYLATION

69
Q

G sub salpha

A

increase phosphorylation

70
Q

G sub i

A

decrease phosphorylation

71
Q

Metabotropic receptor examples

A

Acetylcholine [M], monoamines, peptides

72
Q

M2/M4

A

Increase K+ influx

Decrease adenylyl cyclase

73
Q

M1/M3/M5

A

increase phosphoinositide

74
Q

What can phosphorylation do?

A 
receptor up down regulation
ion channel open/close
Enzyme activation/deactivation
Neurotransmitter release
dendritic growth
cell metabolism
75
Q

Amino acid NT

A

Glutamate GABA Glycine

76
Q

Monoamines

A

Dopamine, Norepinephrine, Epinephrine, and Serotonin

77
Q

Peptides

A

Opioids, Orexin, CRF, BDNF

78
Q

Novel/Gases

A

NO, CO, H2S

79
Q

Purines

A

ATP, Adenosine

80
Q

Catecholamines

A

D, N, E

81
Q

Indoleamine

A

Serotonin

Psychopharmacology (16 decks)

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