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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
what is TrkB
BDNFs receptor
26
what does caffeine to do BDNF and where is this most apparent
increases hippocampal BDNF
27
what are 2 critical roles of BDNF
learning and hippocampal long-term potentiation
28
in what ways does caffeine affect memory
helps with memory consolidation (long term storage)
29
what kind of memory does caffeine NOT effect
retrieval memory
30
does caffeine effect memory consolidation
yes it improves
31
does caffeine effect memory recall
no
32
what dose of caffeine causes a plateau in increased BDNF and TrkB
200mg
33
what does caffeine do to BDNF levels
increase
34
what does caffeine do to TrkB levels
increase
35
what is the molecular mechanism of caffeine
antagonist at adenosine receptors
36
what kind of adenosine receptor is most affected by caffeine
A1 and A2A receptors
37
what is the general role of adenosine
neuromodulator, modulates the release of neurotransmitter via presynaptic receptors
38
where are A1 receptors in the synapse
can be pre or post ganglionic
39
where are A2A receptors in the synapse
can be pre or post ganglionic
40
what G protein is associated with A1 and how/what does it cause
Gi-inhibit adenylyl cyclase so there is less cAMP production
41
what G protein is associated with A2A and how/what does it cause
Gs- stimulate adenylyl cyclase so there is ,ore cAMP production
42
what does A1 do to neurotransmitter release
inhibits
43
what does A2A do to neurotransmitter release
promotes
44
what does A1 do to neurotransmitter release in presence of caffeine
relative increase in neurotransmitter release (prevents adenosine from preventing NT release)
45
what does A2A do to neurotransmitter release in presence of caffeine
relative decrease in neurotransmitter release (prevents adenosine from causing NT release)
46
where are A1 receptors in the brain
throughout- reward pathway, high in hippocampus
47
is A1 or A2A more common
A1!!!!!!
48
where are A2A receptors in the brain
mostly in DA-rich brain regions and olfactory bulb found mostly on GABA releasing neurons also in reward pathway
49
is GABA excitatory or inhibitory
inhibitory
50
why doesnt the effects of A1 and A2A cancel eachother out
they are found in different parts of the brain for the most part
51
which receptor does A1 pair up with, and how many
1 each of A1 and D1
52
which receptor does A2A pair up with, and how many
two each of A2A and D2
53
what does D1 do to cAMP production
increase
54
what does D2 do to cAMP production
decrease
55
how many of each type in the A1 and A2A complex
1
56
how does the amount of adenosine in the brain change throughout the day
increases extracellular concentration until it triggers sleep
57
what causes the adenosine increase throughout the day
thought to be from ATP metabolism in neurons
58
what does stimulation of A2A by adenosine in hypothalamus usually release +cause
releases GABA which inhibits arousal system (thats why adenosine makes you seepy)
59
how does caffeine make you less sleepy
prevents adenosine binding to A2A which prevents GABA release`
60
what are 3 effects of caffeine at high doses
``` inhibits phosphodiesterase (produces high cAMP) inhibits GABA-A receptors (hyper excitable) increases Ca++ channel function ```
61
what happens when caffeine inhibits phosphodiesterase (2 effects)
increase cAMP levels, causes vasodilation and increased contraction of heart muscle (dysrhythmia)
62
what does phosphodiesterase do
metabolizes cAMP
63
what happens once caffeine inhibits GABA-A receptors
hyperexcitable brain
64
what happens when high caffeine increases Ca++ channel function
increase intracellular calcium which increases the work capacity of muscle
65
do all adenesine receptors have to be blocked to cause a behavioural effect
no
66
what are the primary targets of caffeine
A1 and A2A | also phosphodiesterase too
67
what metabolizes caffeine
CYP1A2
68
what are the 3 metabolism products of caffeine
paraxanthine (84%) theobromine (12%) theophylline (4%)
69
what does paraxanthine do
increases lipolysis, elevates glycerol and free fatty acids-causes increase muscle strength
70
what does theobromine do (2)
dilates blood vessels and increase urine volume
71
what does theophylline do
inhibits phosphodiesterase so it increases cAMP - leads to relaxation of airway smooth muscle
72
what does caffeine do to dopamine levels and where
increase DA in nucleus accumbens
73
how does caffeine increase DA levels
blockage A1 receptors (that normally inhibit glu and DA release) - glu stimualtes DA neurons in VTA
74
how does block of A1 receptors that inhibit glu release (by caffeine) increase DA levels
because glu stimualtes DA neurons in VTA
75
what genes cause fast caffeine metabolism
two copies of *1A CYP1A2 gene
76
what genes cause slow caffeine metabolism
1 or 2 copies of *1F CYP1A2 gene
77
what happens if you have caffeine with two copies of *1A
lowers odds of myocardial infarction (1-3 cups is best)
78
what happens if you have caffeine with 1 or 2 copies of *1F
increases odds of myocardial infarction with increased caffeine doses
79
what can caffeine do to bones and how (2 ways)
osteoporosis because it increases urinary excretion of Ca++ and inhibits absorption from diet
80
what can caffeine do to mental health (2 things)
increase panic attack if you have a A2A mutation | maybe good for antidepressants (increase NT levels)
81
who gets panic attacks from caffeine
if you have a A2A mutation
82
why could caffeine be good as an antidepressant
increase NT levels in synapse
83
how is caffeine dose related to parkinsons
dose related (more caffeine is less risk for parkinsons)
84
how could caffeine reduce risk for parkinsons
blockade of A2 receptor (more DA release (inhibition of GABA)), reducing appearance of symptoms -but this could just be masking parkinsons
85
how does dopamine related to parkinsons
DA helps regulate movement, PD is a lack of control
86
what are nootropics
cognitive enhancer
87
what are some nootropics used for clinically
ADHD, alzheimers, stroke, dimentia
88
how do nootropics work
many types and many different NT systems
89
what is memantine and mechanism of action
nootropic | low affinity reversible NMDA receptor antagonist
90
how does memantine help with people with neurodegenration
stops excess activation of NDMA receptors (this can kill neurons)
91
what does memantine do with normal healthy people (2)
decrease backround glu "noise" that leads to distraction | but still allows receptors to be activated when glu is released from nerve ending
92
what are side effects of memantine
confusion dizziness headache constipation body aches
93
what is rivastigmine and mechanism of action
nootropic, acetylcholinesterase inhibitor (inhibits break down of ACh)
94
how does rivastigmine help with people with neurodegeneration
cognitive enhancer because there is usually a loss of ACh releasing neurons
95
what are side effects of rivastigmine
confusion dizziness hallucinations diarrhea seizures irregular heatbeat severe nausea

PMCOL 305 (26 decks)

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