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PMCOL 305 > 6 - methylxanthines and nootropics > Flashcards

6 - methylxanthines and nootropics Flashcards

1
Q

what are the main effects of caffeine

A

motor activation, arousal, concetration and wakefulness

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2
Q

what does caffeine do to the dopamine system

A

potentiate

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3
Q

what kind of compound is caffeine

A

methylxanthine

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4
Q

what does chlorogenic acid do

A

induce production of phase 2 enzymes

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5
Q

what do phase 2 enzymes do

A

help detoxifying various chemicals

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6
Q

what are 4 other substances found in coffee

A

chlorogenic acids, dihydrocaffeic acid, kahweol and cafestol

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7
Q

what does dihydrocaffeic acid do

A

anti-inflammation and improved vascular health (NO release)

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8
Q

how does digydrocaffeic acid improve vascular health

A

increase release of NO

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9
Q

what does NO release do to vessels

A

vasodilate and reduce BP

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10
Q

what class of molecule are kahweol and cafestol

A

diterpenes

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11
Q

what do kahweol and cafestol do

A

induce phase 2 detoxyfying ezmes and increase resistance to oxidative stress (induce various genes)

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12
Q

how does kahweol and cafestol increase resistance to oxidatice stress

A

induction of various genes

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13
Q

what is a negative effect of kahweol and cafestol

A

elevate cholesterol so increase cardiovascular risk

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14
Q

what is guaranine

A

organic compound identical to caffeine

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15
Q

what is meteine

A

organic compound identical to caffeine

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16
Q

where do guaranine and meteine come from

A

yerba mate and guarana plants

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17
Q

what NTs are increased from caffeine

A

NA, glu, DA

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18
Q

what does caffeine do to blood vessels

A

dilate via endothelial NO release

but constrict centrally (CNS)

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19
Q

at what concentration is caffeine a diuretic

A

300mg

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20
Q

how does caffeine work as a diuretic

A

increase blood flow to kidneys, weakens bladder muscles, inhibits resorption of water and sodium

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21
Q

when can constriction of cranial vessels important

A

in treating headaches

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22
Q

can caffeine cause high blood pressure

A

yes and increase heart rate-more common in naive users

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23
Q

is caffeine a cognitive enhancer

A

yes, it leads to positive effects on memory and learning

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24
Q

what receptor does BDNF act at

A

TrkB

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25
Q

what is TrkB

A

BDNFs receptor

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26
Q

what does caffeine to do BDNF and where is this most apparent

A

increases hippocampal BDNF

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27
Q

what are 2 critical roles of BDNF

A

learning and hippocampal long-term potentiation

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28
Q

in what ways does caffeine affect memory

A

helps with memory consolidation (long term storage)

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29
Q

what kind of memory does caffeine NOT effect

A

retrieval memory

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30
Q

does caffeine effect memory consolidation

A

yes it improves

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31
Q

does caffeine effect memory recall

A

no

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32
Q

what dose of caffeine causes a plateau in increased BDNF and TrkB

A

200mg

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33
Q

what does caffeine do to BDNF levels

A

increase

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34
Q

what does caffeine do to TrkB levels

A

increase

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35
Q

what is the molecular mechanism of caffeine

A

antagonist at adenosine receptors

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36
Q

what kind of adenosine receptor is most affected by caffeine

A

A1 and A2A receptors

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37
Q

what is the general role of adenosine

A

neuromodulator, modulates the release of neurotransmitter via presynaptic receptors

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38
Q

where are A1 receptors in the synapse

A

can be pre or post ganglionic

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39
Q

where are A2A receptors in the synapse

A

can be pre or post ganglionic

40
Q

what G protein is associated with A1 and how/what does it cause

A

Gi-inhibit adenylyl cyclase so there is less cAMP production

41
Q

what G protein is associated with A2A and how/what does it cause

A

Gs- stimulate adenylyl cyclase so there is ,ore cAMP production

42
Q

what does A1 do to neurotransmitter release

A

inhibits

43
Q

what does A2A do to neurotransmitter release

A

promotes

44
Q

what does A1 do to neurotransmitter release in presence of caffeine

A

relative increase in neurotransmitter release (prevents adenosine from preventing NT release)

45
Q

what does A2A do to neurotransmitter release in presence of caffeine

A

relative decrease in neurotransmitter release (prevents adenosine from causing NT release)

46
Q

where are A1 receptors in the brain

A

throughout- reward pathway, high in hippocampus

47
Q

is A1 or A2A more common

A

A1!!!!!!

48
Q

where are A2A receptors in the brain

A

mostly in DA-rich brain regions and olfactory bulb
found mostly on GABA releasing neurons
also in reward pathway

49
Q

is GABA excitatory or inhibitory

A

inhibitory

50
Q

why doesnt the effects of A1 and A2A cancel eachother out

A

they are found in different parts of the brain for the most part

51
Q

which receptor does A1 pair up with, and how many

A

1 each of A1 and D1

52
Q

which receptor does A2A pair up with, and how many

A

two each of A2A and D2

53
Q

what does D1 do to cAMP production

A

increase

54
Q

what does D2 do to cAMP production

A

decrease

55
Q

how many of each type in the A1 and A2A complex

A

1

56
Q

how does the amount of adenosine in the brain change throughout the day

A

increases extracellular concentration until it triggers sleep

57
Q

what causes the adenosine increase throughout the day

A

thought to be from ATP metabolism in neurons

58
Q

what does stimulation of A2A by adenosine in hypothalamus usually release +cause

A

releases GABA which inhibits arousal system (thats why adenosine makes you seepy)

59
Q

how does caffeine make you less sleepy

A

prevents adenosine binding to A2A which prevents GABA release`

60
Q

what are 3 effects of caffeine at high doses

A 
inhibits phosphodiesterase (produces high cAMP)
inhibits GABA-A receptors (hyper excitable)
increases Ca++ channel function
61
Q

what happens when caffeine inhibits phosphodiesterase (2 effects)

A

increase cAMP levels, causes vasodilation and increased contraction of heart muscle (dysrhythmia)

62
Q

what does phosphodiesterase do

A

metabolizes cAMP

63
Q

what happens once caffeine inhibits GABA-A receptors

A

hyperexcitable brain

64
Q

what happens when high caffeine increases Ca++ channel function

A

increase intracellular calcium which increases the work capacity of muscle

65
Q

do all adenesine receptors have to be blocked to cause a behavioural effect

A

no

66
Q

what are the primary targets of caffeine

A

A1 and A2A

also phosphodiesterase too

67
Q

what metabolizes caffeine

A

CYP1A2

68
Q

what are the 3 metabolism products of caffeine

A

paraxanthine (84%)
theobromine (12%)
theophylline (4%)

69
Q

what does paraxanthine do

A

increases lipolysis, elevates glycerol and free fatty acids-causes increase muscle strength

70
Q

what does theobromine do (2)

A

dilates blood vessels and increase urine volume

71
Q

what does theophylline do

A

inhibits phosphodiesterase so it increases cAMP - leads to relaxation of airway smooth muscle

72
Q

what does caffeine do to dopamine levels and where

A

increase DA in nucleus accumbens

73
Q

how does caffeine increase DA levels

A

blockage A1 receptors (that normally inhibit glu and DA release) - glu stimualtes DA neurons in VTA

74
Q

how does block of A1 receptors that inhibit glu release (by caffeine) increase DA levels

A

because glu stimualtes DA neurons in VTA

75
Q

what genes cause fast caffeine metabolism

A

two copies of *1A CYP1A2 gene

76
Q

what genes cause slow caffeine metabolism

A

1 or 2 copies of *1F CYP1A2 gene

77
Q

what happens if you have caffeine with two copies of *1A

A

lowers odds of myocardial infarction (1-3 cups is best)

78
Q

what happens if you have caffeine with 1 or 2 copies of *1F

A

increases odds of myocardial infarction with increased caffeine doses

79
Q

what can caffeine do to bones and how (2 ways)

A

osteoporosis because it increases urinary excretion of Ca++ and inhibits absorption from diet

80
Q

what can caffeine do to mental health (2 things)

A

increase panic attack if you have a A2A mutation

maybe good for antidepressants (increase NT levels)

81
Q

who gets panic attacks from caffeine

A

if you have a A2A mutation

82
Q

why could caffeine be good as an antidepressant

A

increase NT levels in synapse

83
Q

how is caffeine dose related to parkinsons

A

dose related (more caffeine is less risk for parkinsons)

84
Q

how could caffeine reduce risk for parkinsons

A

blockade of A2 receptor (more DA release (inhibition of GABA)), reducing appearance of symptoms
-but this could just be masking parkinsons

85
Q

how does dopamine related to parkinsons

A

DA helps regulate movement, PD is a lack of control

86
Q

what are nootropics

A

cognitive enhancer

87
Q

what are some nootropics used for clinically

A

ADHD, alzheimers, stroke, dimentia

88
Q

how do nootropics work

A

many types and many different NT systems

89
Q

what is memantine and mechanism of action

A

nootropic

low affinity reversible NMDA receptor antagonist

90
Q

how does memantine help with people with neurodegenration

A

stops excess activation of NDMA receptors (this can kill neurons)

91
Q

what does memantine do with normal healthy people (2)

A

decrease backround glu “noise” that leads to distraction

but still allows receptors to be activated when glu is released from nerve ending

92
Q

what are side effects of memantine

A

confusion dizziness headache constipation body aches

93
Q

what is rivastigmine and mechanism of action

A

nootropic, acetylcholinesterase inhibitor (inhibits break down of ACh)

94
Q

how does rivastigmine help with people with neurodegeneration

A

cognitive enhancer because there is usually a loss of ACh releasing neurons

95
Q

what are side effects of rivastigmine

A

confusion dizziness hallucinations diarrhea seizures irregular heatbeat severe nausea

PMCOL 305 (26 decks)

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