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PMCOL 305 > nicotine 2 > Flashcards

nicotine 2 Flashcards

1
Q

how many subunits in nicotininc receptor

A

5

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2
Q

how many diff types of alpha and beta subunits in nicotinic receptors

A

9 alpha 3 beta

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3
Q

what happens once the nicotinic receptor is triggered by nicotine

A

integral ion channel opens to let sodium and calcium into the cell (depolarization)

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4
Q

does nicotinic activation cause depolarization or hyperpolarization

A

depol

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5
Q

what kind of receptor is nic receptor

A

integral ion channel

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6
Q

how many binding sites for nicotine in each receptor

A

2 nicotine

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7
Q

where does nicotine bind compared to ACh

A

same place as ACh

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8
Q

are nicotinic receptors pre or post synaptic

A

either

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9
Q

where are nic receptors postsynaptic

A

neuromuscular junction

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10
Q

what happens when postsynaptic nic receptor is activated

A

quickly depolarize and cause neuromuscular excitation

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11
Q

what happens when presynaptic nic receptor is activated

A

induce release of NT glu, GABA, DA, NA, 5HT…

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12
Q

what happens if the nic receptor is continually exposed to agonist

A

quickly desensitizes (Seconds, minutes)

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13
Q

what happens with mutations in alpha 4 subunits in animals

A

they are hyper-sensitive to nicotine

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14
Q

what happens with beta 2 subunit knockout in mice

A

nicotine no longer causes release of dopamine + no more self administration

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15
Q

what happens with alpha4beta2 antagonists

A

rewarding effects of nicotine are gone

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16
Q

what is the most important receptors involved in nicotine related DA release

A

alpha4beta2

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17
Q

what other receptor may be implicated with glutamate release

A

alpha7

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18
Q

what does the alpha7 subunit do

A

may be implicated with glutamate release

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19
Q

where are 2 places where alpha4beta2 are found

A

dopaminergic neuronal cell bodies

nerve terminals that release other NTs

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20
Q

are alpha4beta2 pre or post synaptic

A

both

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21
Q

are alpha4beta2 in the reward pathway? what do they cause

A

yes, cause DA releasing effects

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22
Q

do all nicotinic receptors desensitize the same way

A

no

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23
Q

which nerve endings are alpha4beta2 found on a lot

A

GABA releasing neurons

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24
Q

what happens with alpha4beta2 on GABA releasing neurons and their nicotine sensitivity (how sensitive are they to nicotine)

A

very sensitive to nicotine induced desensitization, desensitize very quick
-decrease GABA release

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25
Q

how long do alpha4beta2 on GABA releasing neurons take to cause desensitization

A

less than 1 min

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26
Q

how long do alpha4beta2 on GABA releasing neurons stay desensitised

A

at least 1 hour

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27
Q

how are GABA releasing neurons affected by nicotine

A

very affected if they have the alpha4beta2

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28
Q

how are glutamate releasing neurons affected by nicotine

A

nicotine activates them, but they still stay functional (alpha7)

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29
Q

which subunit is responsible for nicotines effect on GABA releasing neurons

A

alpha4beta2

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30
Q

which subunit is responsible for nicotines effect on glutamate releasing neurons

A

alpha7

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31
Q

what is the effect on DA due to nicotines effect on GABA releasing neurons

A

indirect stimulation of DA release

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32
Q

what is the effect on DA due to nicotines effect on glu releasing neurons

A

indirect stimulation of DA release

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33
Q

do the alpha4beta2 or alpha7 subunits become nonfunctional with nicotine

A

alpha4beta2

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34
Q

do the alpha4beta2 or alpha7 subunits stay functional with nicotine

A

alpha7

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35
Q

what NTs control dopaminergic neuron firing in the VTA

A

glutamate and GABA

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36
Q

is glutamate excitatory or inhibitory

A

excitatory

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37
Q

what causes the increase of DA release from nicotine (3)

A

more glu release (alpha7) less GABA release (alpha4beta2) onto DA releasing cells on VTA

receptors on cell bodies of DA releasing neurons can be activated by nicotine

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38
Q

when nicotine is applied directly to DA releasing neurons in the VTA, how long do levels remain above baseline

A

80mins

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39
Q

what does nicotine do to neuron firing of the neurons in the mesolimbic pathway

A

increases

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40
Q

what does nicotine do to DA release at the NAc

A

increase

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41
Q

what happens with monoamine oxidase with smoking and how

A

inhibited by cigarette smoke, likely via acetaldehyde

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42
Q

what does monoamine oxidase do

A

breaks down NTs

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43
Q

what may acetaldehyde be forming that is inhibiting monoamine oxidase

A

beta-carbolines

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44
Q

where do beta-carbolines come from

A

acetaldehyde

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45
Q

what do beta-carbolines do

A

inhibit monoamine oxidases

46
Q

what happens when monoamine oxidases are inhibited

A

increased levels of dopamine, adrenaline and noradrenaline

47
Q

how does acetaldehyde from cigarette smoke cause a reinforcing effect of nicotine

A

they form beta carbolines which inhibit monoamine oxidases,cause an increase in DA NA A levels

48
Q

is there more monoamine oxidases in smokers or non smokers

A

more in non smokers (normal level)

49
Q

is there less monoamine oxidases in smokers or non smokers

A

less in smokers (reduced level due to inhibition by beta-carbolines)

50
Q

is nicotine involved in the MAO inhibition

A

no

51
Q

what happens with nicotinic receptor level with chronic nicotine exposure

A

increase number of nicotinic receptors

52
Q

what is the major type of upregulated nicotinic receptor

A

alpha4beta2

53
Q

why are nicotinic receptors upregulated if nicotine is an agonist

A

because they get desensitized by nicotine (rapidly non functional so the brain makes more to compensate for it)

54
Q

is nicotine an agonist or antagonist

A

agonist

55
Q

what will happen to sensitization to effects of nicotine when they are upregulated

A

increased sensitization to the effects of nicotine (especially when receptors are resensitized)

56
Q

where does tar adhere to in the airway

A

cells in the airways

57
Q

what is an example of a carcinogen in tar

A

polycyclic aromatic hydrocarbons

58
Q

why are polycyclic aromatic hydrocarbons dangerous

A

they are planar so can easily insert themsleves between base pairs in DNA

59
Q

what does tar do to cilia in airways

A

inhibits their function

60
Q

what happens to phagocytes in airways

A

function is inhibited

61
Q

what causes polycyclic aromatic hydrocarbons to be produced

A

when proteins burn

62
Q

what is benzo[a]pyrene

A

product of incomplete combustion and a procarcigogen

63
Q

is benzo[a]pyrene a carcinogen

A

no its a procarcinogen

64
Q

how does benzo[a]pyrene become a carcinogen

A

gets metabolized into an active form

65
Q

how is the metabolized form of benzo[a]pyrene a carcinogen (what does it do that makes it a carcinogen)

A

inserts into DNA where it covalently binds to guanine and causes a bulge in the double helix (faulty replication)

66
Q

what kind of modification on benzo[a]pyrene makes it a carcinogen

A

it becomes an epoxide (its probably okay if you dont know this)

67
Q

does nicotine initiate cancer

A

no

68
Q

where can nicotine support pro-cancer effects

A

in non-neuronal cells

69
Q

what are 3 pro-cancer effects that nicotine causes

A

inhibits apoptosis, promotes cell proliferation and can cause mutation

70
Q

how can nicotine cause prevention of apoptosis (which receptors and where)

A

activation of alpha7 receptors on mitochondria can prevent apoptosis

71
Q

how can nicotine cause prevention of apoptosis

A

activation of alpha7 receptors on mitochondria can prevent apoptosis

72
Q

what is dangerous with nicotine induced prevention of apoptosis

A

damaged DNA can keep proliferating

73
Q

what does nicotine do to cancer cells in vitro

A

enhances growth

74
Q

what does nicotine do to cancer cells that are injected into mice

A

promotes growth

75
Q

what does nicotine do to tumor metastasis

A

increase in animal models

76
Q

what does nicotine do to tumor recurrence

A

increase in animal models

77
Q

how did they know that nicotine increase stumor recurrence (how did they do the experiment)

A

mice injected with cancer cells, then got either nicotine or control for 2 weeks, surgically removed tumors, continue with treatment, 2 weeks later there were more tumors and metastasis with nic treated group

78
Q

did the nicotine treated mice have an increase tumor recurrence

A

yes

79
Q

did the nicotine treated mice have an increase tumor metastasis

A

yes

80
Q

which nicotine derivatives are formed during curing and burning

A

NNK and NNN

81
Q

what are NNK and NNN and how are they formed

A

nitrosamines formed by nitrosation of nicotine (formed by curing/smoking)

82
Q

do NNK and NNN directly cause cancer

A

yes

83
Q

do NNK and NNN indirectly cause cancer

A

yes

84
Q

how does NNN and NNK directly cause cancer

A

covalent modification of DNA after further metabolism

85
Q

how does NNN and NNK indirectly cause cancer (2)

A

initiation of proliferation pathways, inhibition of repair pathways (via nAChR)

86
Q

where do NNN and NNK bind and how strong

A

to certain nAChR and more tightly than nicotine

87
Q

are NNN and NNK agonists or antagonist and at which receptor

A

agonists at the nAChR receptor

88
Q

what pathway does NNK affect the most and how

A

increases the proliferation and survival of cells

89
Q

what pathway does NNN affect the most and how

A

decreases motility and wound repair

90
Q

what pathway does NNK and NNN affect together

A

adhesion, indirect modulation, causes metastasis

91
Q

do e cigs smokers contain NNK and NNN

A

yes but 97% lower than cig smokers

92
Q

if NNK and NNN were only formed by curing/smoking, how do e cig users have some in their body

A

nic may get directly metabolized into NNK and NNN in the body by P450 enzymes

93
Q

how were mice’s bodies converting nic into NNK and NNN

A

by P450 enzymes

94
Q

what was evidence of NNK and NNN presence found in mice

A

DNA modifications

95
Q

can exposure to e cig smoke induce lung cancer in mice studies

A

yes

96
Q

what was the original use for bupropion (zyban)

A

antidepressant

97
Q

what does bupropion (zyban) do to help with nicotine addiction (2 thing)

A

moderate increase in DA and NA levels (inhibites removal from synapse and increase release)
locks nicotinic into closed state

98
Q

what does bupropion (zyban) do to NA levels

A

increase

99
Q

what does bupropion (zyban) do to DA levels

A

increase

100
Q

what does bupropion (zyban) do to NA and DA removal from synapse

A

inhibits their removal

101
Q

what does bupropion (zyban) do to NA and DA release

A

increase

102
Q

what does bupropion (zyban) do to nicotinic receptors (+ what is the effect of this)

A

locks them into a closed state

prevents ions from entering its channel even with nic present

103
Q

where does bupropion (zyban) bind to

A

the nicotine channel itself

104
Q

can bupropion (zyban) help with cravings

A

yes

105
Q

what is sucess rate ofbupropion (zyban) after a year

A

30%

106
Q

what is varenicline (champix) mechanism of action

A

partial agonist at alpha4beta2 receptors

107
Q

what activation % does varenicline (champix) do and to what receptors

A

30-60% activation of alpha4/beta2 receptors

108
Q

what does varenicline (champix) do to the effects of nicotine added to the system

A

blocks the effects

109
Q

what does varenicline (champix) do to craving and reinforcing effects of nic and how

A

reduces because it partially substitutes for nicotine

110
Q

what is a downside of varenicline (champix)

A

increase suicide risk, aggression, hostility

111
Q

what happens if you drink while on varenicline (champix)

A

it may make neuropsychiatric events worse

112
Q

what is the 6 month success rate of varenicline (champix)

A

14% eek

PMCOL 305 (26 decks)

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