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Psychopharmacology > Stimulants > Flashcards

Stimulants Flashcards

1
Q

What types of transmitters do amphetamine & cocaine effect?

A

all monoamines!

DA, NE, EPI, 5-HT

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2
Q

What happens when stimulants are used at low doses?

A

Increased attention / mood

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3
Q

What happens when stimulants are used at higher doses?

A

Decreased activity / mood

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4
Q

What happens with chronic high doses of stimulants?

A

Schizophrenia-like state

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5
Q

What are the differences between schizophrenic brains and chronic stimulant brains?

A

Schizophrenic brains have lower DA concentrations in some parts

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6
Q

How long does it take to remove symptoms with antipsychotics in stimulant-induced psychotic states?

Schizophrenia-induced?

A

Stimulant-induced: Hours

Schizophrenia-induced: Weeks

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7
Q

What effects will tolerate with stimulants? Why?

A

Reinforcing effects

Due to regionally specific receptor downregulation at postsynaptic sites

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8
Q

What effects will sensitize with stimulants?

Why?

A

Motor and psychosis-inducing effects

Due to downregulation of presynaptic autoreceptors

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9
Q

What breaks down monoamines?

A

MAO (monoamine oxidase)

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10
Q

What is the ED50 of amphetamine?

A

10mg (narcolepsy)
20-30mg (adhd)
250mg (abuse)

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11
Q

What is the LD50 of amphetamine?

A

200mg

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12
Q

What is the TI of amphetamine?

A

7-15

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13
Q

What is TI?

A

LD50 / ED50

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14
Q

What is the half-life of cocaine?

A

60min

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15
Q

What is the ED50 of cocaine?

A

~3mg dose

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16
Q

What is the LD50 of cocaine?

A

~50mg

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17
Q

What is the TI of cocaine?

A

~15

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18
Q

What are the effects of amphetamine?

A

Increase release of newly-synthasized DA

Cause vesicles to release DA into cytoplasm

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19
Q

What does amph do to DT (dopamine transporter)?

A

Phosphorylates it

DA is then pumped out of the cell

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20
Q

What does Amphetamine block?

A

MAO

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21
Q

What is MAO?

A

monoamine oxidase

Degradation enzyme responsible for inactivating monoamines

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22
Q

What does cocaine do?

A

Blocks transporter (compared to amphetamine, which reverses it)

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23
Q

What is the crucial difference between cocaine / amphetamine?

A

You need action potentials with cocaine

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24
Q

What does cocaine do if near a sodium channel?

A

Blocks it (local anesthetic)

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25
Q

What does cocaine do if near a 5-HT transporter?

A

Blocks it (and other monoamine transporters)

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26
Q

Why doesn’t cocaine always block ion channels, so that it doesn’t have an effect at the synapse?

A

You need much higher concentrations of cocaine to block ion channels

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27
Q

What is the medial forebrain bundle?

A

Axons from the midbrain to the forebrain
mesoaccumbens axons
mesocortical axons
mesolimbic axons

Monoamine projections to the forebrain

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28
Q

How (generally) do amphetamines help with ADHD?

A

Interaction between NE and DA

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29
Q

What are synapses en passante?

A

Synapses ‘in passing’

Swelling in the middle of an axon containing voltage-gated Ca2+ channels

Cause release sites in the axon itself

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30
Q

What is Volume Conduction?

A

Communication not specific to a synapse

Release neurotransmitter into extracellular space, making a ‘gradient’ of changed activation

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31
Q

What are the most diverse group of ion channels?

A

K+ channels

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32
Q

What is a current shunt?

Na+ shunt, K+ shunt

A

As quickly as Na+ comes in, K+ goes out (K+ driving force affected by Na+)

Keeps membrane voltage stable

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33
Q

What are EPSPs in relation to shunts?

A

Overwhelming the ability of the leak channels to compensate for Na+

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34
Q

What is the general rule for D1/D2 receptors?

A 
D1 = excitatory
D2 = inhibitory
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35
Q

What is the effect of blocking shunt for NE/DA in relation to ADHD?

A

Signals better able to come in

Noise blocked

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36
Q

What is a metaphor for increasing NE release for a state-change?

A

Increase volume: make signal stronger, noise weaker

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37
Q

What’s happening in the neuron when you change signal-to-noise by adding amphetamine?

A

Less random activation (shunts, DA)
Cell is more excitable (state-change, depolarization)

Higher likelihood of action potential, but less random noise

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38
Q

How addictive are psychostimulants?

A

Among the most readily addictive substances known

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39
Q

What happens when you have low levels of D4 receptors?

A

‘need the buzz you get from seeing what’s over the next mountain’

More apt to explore, more apt to desire novel experiences

40
Q

How do NE transporters relate to DA?

A

They’re great at picking up DA - can reduce DA levels

Only one enzyme away from NE

41
Q

How to DA transporters relate to NE?

A

Not great at picking up NE

NE is already farther along in the cascade chain than DA, so you can’t synthesize DA from NE

42
Q

How much caffeine does a 6-oz cup of coffee have?

A

74-83mg/5-oz cup (tall is 12-oz)

43
Q

What might help in infant sleep apnea?

A

Caffeine

44
Q

Which receptors does caffeine antagonize?

A

A-1 and A-2Aa adenosine receptors

45
Q

Where are the adenosine receptors we’re interested found?

A

Terminal boutons

But they’re there all over the nervous system

46
Q

Where is adenosine released?

A

Postsynaptically, propagates BACKWARD to terminal bouton

47
Q

What do A-1 receptors do when activated?

A

2nd messenger

Increase K+ efflux
Decrease Ca2+ influx

(decrease exocytosis)

48
Q

Where are there lots of A1 receptors?

A

HC, striatum, septum, frontal/cingulate cortex

49
Q

What brain region is affected first in Alzheimer’s?

A

Septum

50
Q

What type of neurons mainly exist in the septum?

A

Cholinergic

51
Q

What is a higher dose of caffeine?

A

~500mg+

52
Q

What can caffeine do at higher doses?

A

Hallucinations, paranoia, mania/depression

53
Q

Where in the brain is caffeine less potent?

A

Brainstem

2-10 cups

54
Q

Where in the brain is caffeine not very potent?

A

Spinal cord - need 20-50 cups (tremor/seizures)

55
Q

What is the LD50 of caffeine?

A

~200 cups of coffee (15g)

56
Q

Where is caffeine metabolized?

A

Cytochrome p-450 in the liver, excreted in urine

Overlaps with alcohol breakdown enzymes

57
Q

What are the three significant metabolites of caffeine?

A

Paraxanthine (lose a methyl group at the top right)
Theobromine (lose a methyl group between ketones)
Theophylline (lose a methyl group on the bottom left)

58
Q

How does cocaine absorption compare to amphetamine?

A

It’s worse (less fat-soluble)

59
Q

How is the “signal” increased in signal-to-noise by amphetamine?

A

Blocking the NeT

60
Q

What does blocking the NeT by amphetamines do physically in the PfC to strengthen “signal”?

A

NE increases effect transmitters like GLU have at synapses

61
Q

How is “noise” decreased by amphetamine?

A

Blocks DAT

62
Q

How does blocking DAT decrease “noise”?

A

cAMP alteration in ion channels (primarily K+)

Suppresses K+ conductance that normally amplifies irrelevant inputs

63
Q

How popular is nicotine?

A

3 most used drug in the world

64
Q

What is the current therapeutic relevance of nicotine?

A

NO relevance
(Reduces nicotine withdrawal…)

may help tourette’s, parkinson’s, alzheimer’s, schizophrenia

65
Q

Where do you lose cholinergic neurons with alzheimer’s?

A

Septum

66
Q

What does nicotine do?

A

Cholinergic agonist

67
Q

Differences between ACh and Glu?

A

Glutamate is everywhere, has refined effect of NDMA

Ach is very specific to specific parts of the brain (e.g. cholinergic neurons of the septum)

68
Q

How is nicotine usually injested?

A

Orally or by inhalation

69
Q

What is the solubility of nicotine?

A

Both fat and water-soluble

70
Q

How fast does nicotine hit the brain with inhalation?

A

3 min

peak levels within 10 min

71
Q

What is the ED50 of nicotine?

A

.5-1mg

cigarette is 8mg

72
Q

What is first-pass metabolism like for nicotine?

A

HIGH. 90% metabolized in liver by cytochrome P450

73
Q

In what medium is nicotine eliminated?

A

Urine

74
Q

What is the half life of nicotine?

A

1/2 hr

75
Q

Why does tolerance to nicotine develop in the liver?

A

hepatic enzyme activation

76
Q

What is the LD50 of nicotine?

A

60mg

77
Q

What are lethal effects of nicotine produced by?

A

Paralysis of respiratory muscles

Nicotinic receptors get overstimulated

78
Q

What happens to quiescent (dormant) nAchRs in the presence of nicotine?

A

Upregulated, they’re activated

79
Q

What happens in ongoing activation of nAChRs by nicotine?

A

Desensitizes ongoing activation

Acting as an antagonist now

80
Q

How does long-term antagonistic effects of nicotine work?

A

Nicotine pushes receptors into an inactive state after long enough exposure

81
Q

Where in the pons do you see lots of nitcotinic Ach receptors?

A

Locus coeruleus

Lots of NE released there

82
Q

What is causing the rewarding effects of nicotine?

A

Stimulation of mesolimbic DA neurons by nicotinic cholinergic neurons

83
Q

What is the chemical source of arousal by nicotine?

A

nACh activation of LC/Brainstem neurons involved in sleep/wake

Activation of cortical/thalamic neurons

84
Q

What does amphetamine do to MAO?

A

Blocks it, this increases synaptic DA levels

85
Q

Why might amphetamine and cocaine cause toleration of rewarding/reinforcing effects?

A

Not as many DA receptors in specific parts of the brain

86
Q

What is cocaines’ solubility like?

A

Less lipid soluble than amphetamine

Both lipid and water soluble (facilitate entering brain)

87
Q

Which monoamine transporters does cocaine block?

A

5-HT, DA

88
Q

Cocaine acts as a local anesthetic. What does it do to ion channels that causes this?

A

Gets charged (+)

When it’s charged (+), gets stuck inside sodium channels, blocking Na+ from entering

89
Q

What is DATKi? How is it relevant to cocaine?

A

A knock-in DA transporter not sensitive to cocaine

Cocaine doesn’t block it, so it recycles DA just as easily, so cocaine has less effect

90
Q

How fast is the GI absorption of caffeine?

A

99% in 45 min (fast)

91
Q

How fast is the GI absorption of caffeine?

A

99% in 45 min (fast)

92
Q

Where are A1 and A-2a found?

A

presynaptically (terminal boutons)

93
Q

What happens when adenosine binds to A-1 receptors?

A

2nd messenger signals increase K+ efflux, decrease Ca2+ influx

This decreases exocytosis

94
Q

Where in the brain are A-1 receptors generally found?

A

Limbic + memory system:

HC, striatum, septum, frontal/cingulate cortex

95
Q

The neurons of which part of the brain does caffeine have the greatest effect on?

A

Cortical neurons - big increase in cortical activity

Psychopharmacology (12 decks)

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