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PSYC 211 > Lecture 7: Psychopharmacology & Drugs > Flashcards

Lecture 7: Psychopharmacology & Drugs Flashcards

1
Q

most of our knowledge of drugs and neurotransmitter signalling came from studying

A

snake and spider venom

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2
Q

motor neurons release ___ as their main neurotransmitter

A

acetylcholine

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3
Q

sensory neurons release ____ as their main neurotransmitter

A

glutamate

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4
Q

in the CNS acetylcholine has ___ receptors often located at ___

A

ionotropic & metabotropic receptors, axoaxonic synapses

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5
Q

in the PNS acetylcholine has ____ receptors often located at ____

A

ionotropic receptors, neuromuscular junction

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6
Q

poison produced by the black widow spider triggers the release of ___

A

acetylcholine

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7
Q

can people survive the bite of a black widow spider?

A

the average healthy person can

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8
Q

how is botulinum toxin (botox) produced?

A

produced by bacteria that grow in improperly canned food

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9
Q

how does botox affect acetylcholine?

A

it prevents the release of acetylcholine

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10
Q

how does botox prevent wrinkles

A

as you age, motor neurons begin to leak and release acetylcholine without action potentials, causing wrinkling. by inhibiting acetylcholine, botox prevents motor neurons from leaking

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11
Q

how does neostigmine affect acetylcholine?

A

it inhibits the activity of acetylcholinesterase, the enzyme that breaks down acetylcholine in the synaptic cleft. this makes acetylcholine hang around for longer in synapses, causing muscles to stay contracted.

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12
Q

what is myasthenia gravis?

A

a hereditary autoimmune disorder in which the person’s immune system attacks their healthy acetylcholine receptors. symptoms include increasing fatigability

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13
Q

what is the cure for myasthenia gravis?

A

neostigmine can make the released acetylcholine stay around for longer periods, decreasing fatigability

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14
Q

drug

A

An exogenous chemical (comes from outside the body) that at relatively low doses significantly alters the function of certain cells.

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15
Q

Psychopharmacology

A

Study of effects of drugs on the nervous system and behaviour

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16
Q

drug effect

A

The changes a drug produces on physiological processes and behaviour

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17
Q

site of action

A

Location at which molecules of a drug interact with molecules located on or in cells of the body, affecting some biochemical processes of these cells

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18
Q

does the definition of a drug apply to alcohol?

A

no because it doesn’t have much of an effect in small doses

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19
Q

what receptors allow drugs to work

A

ligand recpetors

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20
Q

antipsychotics

A

class of drugs used to treat psychosis

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21
Q

dirty drugs

A

bind to more than one type of receptor

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22
Q

what type of drugs are antipsychotics

A

dirty drugs (they bind to more than one type of receptor)

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23
Q

what is psychosis and what are the symptoms?

A

an abnormal condition of the mind that results in difficulties determining what is real and what is not real. symptoms include delusions, hallucinations, incoherent speech, and inappropriate behaviour

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24
Q

how do antipsychotics work?

A

they directly block the dopamine D2 receptor (inhibitory metabotropic receptor) expressed by neurons all over the brain

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25
Q

what type of a receptor is dopamine D2

A

inhibitory metabotropic receptor

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26
Q

how do hallucinogens work

A

most street hallucinogens directly activate serotonin 2A receptors, which are inhibitory metabotropic receptors expressed by neurons all over the brain

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27
Q

what type of receptor is serotonin 2A

A

inhibitory metabotropic receptor

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28
Q

why do some drugs that activate serotonin 2A not cause hallucinations?

A

hallucinogenic drugs stimulate serotonin 2A in a slightly different way (they add a g protein called Gio). the activation of Gio is what causes hallucinations

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29
Q

biased agonism

A

When a metabotropic receptor ligand causes the receptor to preferentially activate one type of intracellular g protein whereas another ligand at the same receptor might preferentially activate a different g protein

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30
Q

Sasha Shulgin

A

godfather of ecstasy

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31
Q

how do we typically define drugs?

A

by how they affect postsynaptic receptor activity (directly or indirectly)

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32
Q

direct agonists/antagonists

A

drugs that affect postsynaptic receptor activity by directly binding to postsynaptic receptors

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33
Q

indirect agonists/ antagonists

A

drugs taht indirectly affect postsynaptic receptor activity. the proteins they bind to are not postsynaptic receptors

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34
Q

receptor agonist

A

a drug that directly or indirectly increases the activity of postsynaptic receptor proteins

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35
Q

receptor antagonist

A

A drug that directly or indirectly decreases the activity of postsynaptic receptor proteins.

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36
Q

4 different ways to categorize drugs

A
  1. According to their behavioural effects (e.g., upper, downer, stimulant)
  2. According to their physiological effects (e.g., action potential blocker)
  3. According to their actions on specific proteins (e.g., serotonin reuptake blocker)
  4. According to their effects on postsynaptic receptor activity
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37
Q

competitive binding

A

binds to the postsynaptic receptor directly

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38
Q

competitive agonist

A

activates the receptor by binding where the neurotransmitter normally binds

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39
Q

competitive antagonist

A

attaches to the same binding where the neurotransmitter normally binds, but it doesn’t activate the receptor

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40
Q

competitive agonists are ___ agonists

A

full or partial

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41
Q

competitive antagonists are ____ antagonists

A

full

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42
Q

the competition for a binding site between an endogenous neurotransmitter and an exogenous drug will depend on

A

their concentration and affinity for the binding site

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43
Q

affinity

A

the probability and tightness of a ligand-receptor binding

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44
Q

non-competitive binding

A

binds to a receptor at a site that does not interfere with the binding site of the principal ligand (neurotransmitter)

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45
Q

t or f: a neurotransmitter can bind on one site of a receptor while a drug binds on anotehr

A

true

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46
Q

non-competitive agonist

A

fully or partially activates the receptor

47
Q

non-competitive antagonist

A

fully blocks receptor actiavtion. it doesn’t compete for the neurotransmitter binding site, it automatically wins

48
Q

allosteric modulators

A

non-competitive drugs that only influence receptor activity when the neurotransmitter is also bound to the receptor

49
Q

negative allosteric modulators

A

reduce the effect of the primary ligand (neurotransmitter)

50
Q

positive allosteric modulators

A

amplify the effect of the primary ligand (neurotransmitter)

51
Q

Parkinson’s disease

A

a neurological disorder that is characterized by tremors, rigidity of limbs, poor balance, and difficulty initiating movements
It is caused by degeneration (death) of dopamine neurons in the midbrain

52
Q

how to help with the symptoms of Parkinson’s

A

inject the enzyme L-DOPA. it increases dopamine production in the brain and thus acts as an indirect dopamine receptor agonist

53
Q

where are conventional neurotransmitters made?

A

in axon terminals/ they are made from precursor molecules

54
Q

t or f: In some cases, precursor molecules can be administered as drugs since they can increase the amount of neurotransmitter that is made and released

A

true (ex. L-DOPA)

55
Q

The synthesis of neurotransmitters from precursor molecules is controlled by

A

enzymes

56
Q

Once made, neurotransmitters are

A

packaged into synaptic vesicles

57
Q

Many proteins in the axon terminal regulate

A

synaptic vesicle exocytosis (i.e. vesicle fusion with the presynaptic membrane)

58
Q

antagonists prevent the release of neurotransmitter by

A

blocking the vesicular release machinery

59
Q

agonists increase the release of neurotransmitters by

A

binding and activating the vesicular release machinery to directly cause the release of neurotransmitters

60
Q

The clearance of neurotransmitters from the synapse is controlled by

A

reuptake transporter proteins and enzymatic deactivation

61
Q

do agonists block enzymatic deactiavtion and neurotransmitter reuptake proteins?

A

some block the enzymatic deactivation, others block neurotransmitter reuptake proteins

62
Q

what do Methylphenidate (Ritalin) & cocaine: block?

A

dopamine and norepinephrine (catecholamine neutrotransmitter) reuptake transporters

63
Q

what do addreall and crystal meth reverse?

A

catecholamine transporters, causing dopamine and norepinephrine to flow directly out of the presynaptic terminal

64
Q

dose response curve

A

A graph of the magnitude of an effect of a drug as a function of the amount that is administered.

65
Q

margin of safety

A

the difference between the two curves of the drugs. The ratio between the dose that produces a toxic event in 50% of animals and the dose that produces the desired effect in 50% of animals

66
Q

pharmacokinetics

A

The process by which drugs are absorbed, distributed within the body, broken down, and excreted

67
Q

3 considerations when choosing a route of drug administration

A
  1. does the drug naturally cross the blood-brain barrier?
  2. is it better to have a high concentration of drug for a short time or a low concentration of drug for a long time?
  3. where in the body are the enzymes that break down the drug?
68
Q

intravenous administration

A

injection into the vein

69
Q

lntraperitoneal administration

A

injection into the abdominal wall (peritoneal cavity)

70
Q

intramuscular administration

A

injection into the msucle

71
Q

subcutaneous administration

A

injection into the space between the skin

72
Q

oral administration

A

by mouth

73
Q

sublingual administration

A

under the toungue (lots of blood vessels there, so it can be absorbed)

74
Q

intrarectal administration

A

in the rectum as a suppository

75
Q

inhalation

A

by smoking

76
Q

topical administration

A

on the skin

77
Q

intracerebral administration

A

directly into the brain

78
Q

intracerebroventricular administration

A

into a cerebral ventricle

79
Q

intrathecal (epidural) administration

A

into the cerebrospinal fluid of the spinal cord

80
Q

acetylcholinesterase

A

the enzyme that breaks down acetylcholine in the synaptic cleft

81
Q

Direct agonists/antagonists can be classified as

A

competitive or non-competitive

82
Q

types of allosteric modulators

A

negative and positive

83
Q

synaptic vesicle exocytosis

A

vesicle fusion with the presynaptic membrane

84
Q

botox is an __

A

acetylcholine antagonist

85
Q

black widow spider venom is an ___

A

indirect acetylcholine agonist

86
Q

why is heroin more addictive than other opiates like morphine & Imodium anti-diarrheal?

A

heroin crosses the blood-brain barrier quickly (it’s very lipid soluble), whereas morphine crosses it slowly and Immodium anti-diarrheal doesn’t cross it at all

87
Q

what makes certain drugs more likely to cross the blood-brain barrier?

A

more lipid soluble = crosses the blood-brain barrier quicker

88
Q

tolerance

A

when the effects of a drug decrease because of repeated administration. the body attempts to compensate for the effects of the drug

89
Q

withdrawal symptoms

A

opposite effects of the drug

90
Q

why are barbiturates particularly dangerous?

A

their sedative effects show tolerance, but their depressive effects don’t

91
Q

do sedative effects show tolerance?

A

yes

92
Q

do depressive effects show tolerance?

A

no

93
Q

sensitization

A

occurs when a drug becomes more effective through repeated use (opposite of tolerance)

94
Q

Placebo

A

an inert substance that has no direct physiological effect. it is given to subjects to control the effects of a mere administration of a drug

95
Q

exogenous substance

A

comes from outside the body

96
Q

endogenous substance`

A

comes from inside the body

97
Q

what do agonists do?

A

increase the normal activity of a given neurotransmitter

98
Q

what do antagonists do?

A

decrease the normal activity of a given neurotransmitter

99
Q

partial agonists

A

slightly bind to the receptor (less potent agonist)

100
Q

how do competitive partial agonists behave when receptor activity is low?

A

they act like agonists

101
Q

how do competitive partial agonists behave when receptor activity is high?

A

they act like antagonists

102
Q

L-DOPA makes

A

individual neurons release more dopamine

103
Q

neuropeptides are responsible for

A

pleasure and analgesia (inability to feel pain)

104
Q

example of neuropeptide

A

opiods

105
Q

lipid-based signalling molecules are responsible for

A

presynaptic regulation

106
Q

acetylcholine is responsible for

A

attention and memory

107
Q

high affinity = __ dose to acheive efffect

A

low

108
Q

low affinity = ___ dose to achieve effect

A

high

109
Q

how quickly does intravenous injection reach blood plasma?

A

direct and quick

110
Q

how quickly does topical injection reach blood plasma?

A

indirect and slow

111
Q

how quickly does inhalation reach blood plasma?

A

less direct & moderate

112
Q

effect of higher affinity on a drug response curve

A

shifted left

113
Q

effect of lower affinity on a drug response curve

A

shifted right

PSYC 211 (23 decks)

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