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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
what type of a receptor is dopamine D2
inhibitory metabotropic receptor
26
how do hallucinogens work
most street hallucinogens directly activate serotonin 2A receptors, which are inhibitory metabotropic receptors expressed by neurons all over the brain
27
what type of receptor is serotonin 2A
inhibitory metabotropic receptor
28
why do some drugs that activate serotonin 2A not cause hallucinations?
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
29
biased agonism
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
30
Sasha Shulgin
godfather of ecstasy
31
how do we typically define drugs?
by how they affect postsynaptic receptor activity (directly or indirectly)
32
direct agonists/antagonists
drugs that affect postsynaptic receptor activity by directly binding to postsynaptic receptors
33
indirect agonists/ antagonists
drugs taht indirectly affect postsynaptic receptor activity. the proteins they bind to are not postsynaptic receptors
34
receptor agonist
a drug that directly or indirectly increases the activity of postsynaptic receptor proteins
35
receptor antagonist
A drug that directly or indirectly decreases the activity of postsynaptic receptor proteins.
36
4 different ways to categorize drugs
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
37
competitive binding
binds to the postsynaptic receptor directly
38
competitive agonist
activates the receptor by binding where the neurotransmitter normally binds
39
competitive antagonist
attaches to the same binding where the neurotransmitter normally binds, but it doesn't activate the receptor
40
competitive agonists are ___ agonists
full or partial
41
competitive antagonists are ____ antagonists
full
42
the competition for a binding site between an endogenous neurotransmitter and an exogenous drug will depend on
their concentration and affinity for the binding site
43
affinity
the probability and tightness of a ligand-receptor binding
44
non-competitive binding
binds to a receptor at a site that does not interfere with the binding site of the principal ligand (neurotransmitter)
45
t or f: a neurotransmitter can bind on one site of a receptor while a drug binds on anotehr
true
46
non-competitive agonist
fully or partially activates the receptor
47
non-competitive antagonist
fully blocks receptor actiavtion. it doesn't compete for the neurotransmitter binding site, it automatically wins
48
allosteric modulators
non-competitive drugs that only influence receptor activity when the neurotransmitter is also bound to the receptor
49
negative allosteric modulators
reduce the effect of the primary ligand (neurotransmitter)
50
positive allosteric modulators
amplify the effect of the primary ligand (neurotransmitter)
51
Parkinson's disease
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
how to help with the symptoms of Parkinson's
inject the enzyme L-DOPA. it increases dopamine production in the brain and thus acts as an indirect dopamine receptor agonist
53
where are conventional neurotransmitters made?
in axon terminals/ they are made from precursor molecules
54
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
true (ex. L-DOPA)
55
The synthesis of neurotransmitters from precursor molecules is controlled by
enzymes
56
Once made, neurotransmitters are
packaged into synaptic vesicles
57
Many proteins in the axon terminal regulate
synaptic vesicle exocytosis (i.e. vesicle fusion with the presynaptic membrane)
58
antagonists prevent the release of neurotransmitter by
blocking the vesicular release machinery
59
agonists increase the release of neurotransmitters by
binding and activating the vesicular release machinery to directly cause the release of neurotransmitters
60
The clearance of neurotransmitters from the synapse is controlled by
reuptake transporter proteins and enzymatic deactivation
61
do agonists block enzymatic deactiavtion and neurotransmitter reuptake proteins?
some block the enzymatic deactivation, others block neurotransmitter reuptake proteins
62
what do Methylphenidate (Ritalin) & cocaine: block?
dopamine and norepinephrine (catecholamine neutrotransmitter) reuptake transporters
63
what do addreall and crystal meth reverse?
catecholamine transporters, causing dopamine and norepinephrine to flow directly out of the presynaptic terminal
64
dose response curve
A graph of the magnitude of an effect of a drug as a function of the amount that is administered.
65
margin of safety
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
pharmacokinetics
The process by which drugs are absorbed, distributed within the body, broken down, and excreted
67
3 considerations when choosing a route of drug administration
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
intravenous administration
injection into the vein
69
lntraperitoneal administration
injection into the abdominal wall (peritoneal cavity)
70
intramuscular administration
injection into the msucle
71
subcutaneous administration
injection into the space between the skin
72
oral administration
by mouth
73
sublingual administration
under the toungue (lots of blood vessels there, so it can be absorbed)
74
intrarectal administration
in the rectum as a suppository
75
inhalation
by smoking
76
topical administration
on the skin
77
intracerebral administration
directly into the brain
78
intracerebroventricular administration
into a cerebral ventricle
79
intrathecal (epidural) administration
into the cerebrospinal fluid of the spinal cord
80
acetylcholinesterase
the enzyme that breaks down acetylcholine in the synaptic cleft
81
Direct agonists/antagonists can be classified as
competitive or non-competitive
82
types of allosteric modulators
negative and positive
83
synaptic vesicle exocytosis
vesicle fusion with the presynaptic membrane
84
botox is an __
acetylcholine antagonist
85
black widow spider venom is an ___
indirect acetylcholine agonist
86
why is heroin more addictive than other opiates like morphine & Imodium anti-diarrheal?
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
what makes certain drugs more likely to cross the blood-brain barrier?
more lipid soluble = crosses the blood-brain barrier quicker
88
tolerance
when the effects of a drug decrease because of repeated administration. the body attempts to compensate for the effects of the drug
89
withdrawal symptoms
opposite effects of the drug
90
why are barbiturates particularly dangerous?
their sedative effects show tolerance, but their depressive effects don't
91
do sedative effects show tolerance?
yes
92
do depressive effects show tolerance?
no
93
sensitization
occurs when a drug becomes more effective through repeated use (opposite of tolerance)
94
Placebo
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
exogenous substance
comes from outside the body
96
endogenous substance`
comes from inside the body
97
what do agonists do?
increase the normal activity of a given neurotransmitter
98
what do antagonists do?
decrease the normal activity of a given neurotransmitter
99
partial agonists
slightly bind to the receptor (less potent agonist)
100
how do competitive partial agonists behave when receptor activity is low?
they act like agonists
101
how do competitive partial agonists behave when receptor activity is high?
they act like antagonists
102
L-DOPA makes
individual neurons release more dopamine
103
neuropeptides are responsible for
pleasure and analgesia (inability to feel pain)
104
example of neuropeptide
opiods
105
lipid-based signalling molecules are responsible for
presynaptic regulation
106
acetylcholine is responsible for
attention and memory
107
high affinity = __ dose to acheive efffect
low
108
low affinity = ___ dose to achieve effect
high
109
how quickly does intravenous injection reach blood plasma?
direct and quick
110
how quickly does topical injection reach blood plasma?
indirect and slow
111
how quickly does inhalation reach blood plasma?
less direct & moderate
112
effect of higher affinity on a drug response curve
shifted left
113
effect of lower affinity on a drug response curve
shifted right

PSYC 211 (23 decks)

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