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PMCOL 305 > alcohol 2 > Flashcards

alcohol 2 Flashcards

1
Q

what kind of receptors are GABA A

A

ligand gated ion channel

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2
Q

what happens when GABA A are activated

A

ion channel opens and Cl- flows in

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3
Q

how many subunits in GABA receptor

A

5

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4
Q

what happens to the cell once Cl- enters cell via GABA receptor

A

hyperpolarizes the membrane/ inhibits depolarization

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5
Q

what are the most common subunits in GABA receptors

and how many kinds of each

A

alpha (6 kinds)
beta (4)
gamma (3)
delta

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6
Q

what are the constant and variable types of receptors in GABA

A

2 alpha 2 beta always

then gamma or delta

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7
Q

where does GABA bind

A

at interface between alpha and beta subuntits

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8
Q

what does alcohol do to GABA

A

potentiates the effects of GABA

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9
Q

which receptor is most likely included in GABA when it is most effected by alcohol

A

delta

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10
Q

which subunits respond to low ethanol levels that most humans would experience

A

delta

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11
Q

what region of the GABA receptor does ethanol interact with

A

in the receptor that interfaces with lipid bilayer

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12
Q

what does ethanol do to Cl- influx into cell (via GABA)

A

it increases Cl- influx into the cell

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13
Q

what happens when a single GABA molecule goes to the receptor

A

not much, usually need 2

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14
Q

are there more Cl- usually on inside or outside of cell

A

more on outside

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15
Q

what synthetic molecule activated NMDA receptors

A

N-methyl D aspartate (NMDA)

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16
Q

what are the subunits for NMDA receptors (how many of each)

A

4 per receptor

  • two NR1 (essential)
  • two of any NR2 (A B C or D)
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17
Q

where does glutamate bind

A

not at the subunit interface

but more on the sides kinda

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18
Q

does glutamate bind at the subunit interface

A

no

more on the sides

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19
Q

what happens when NMDA receptors are activated

A

Na+ and Ca2+ ion channel opens and they enter the cell

-depolarization

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20
Q

does depolarization or hyperpolarization happen with NMDA activation

A

depolarization

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21
Q

does depolarization or hyperpolarization happen with GABA Areceptor activation

A

hyperpolarization

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22
Q

what does ethanol do to NMDA

A

inhibits them at high concentrations

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23
Q

what concentrations of ethanol are required to inhibit the NMDA receptor

A

high

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24
Q

are higher concentrations of ethanol required to affect the GABA or the NMDA pump

A

higher concentrations are required to inhibit the NMDA receptor than activate the GABA receptor

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25
Q

where does ethanol bind on the NMDA receptor

A

NOT the same as where NMDA binds

probably in transmembrane domains that interface with the lipid bilayer

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26
Q

what can be dangerous with NMDA receptors

A

excess activation, leading to excitotoxicity due to excess calcium

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27
Q

what is excitotoxicity

A

when NMDA receptors are over stimulated so excess ca enters and becomes toxic

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28
Q

what could cause the neuronal loss seen in alcoholics

A

too much ca entering the cell, excitotoxicity (excess NMDA activation)

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29
Q

does GABA R or NMDA R have more subunits

A

GABA - 5

NMDA - 4

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30
Q

where are the GABA A R with delta

A

not actually in synaptic left, more in like axons and dendrites and even cell body

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31
Q

what does ethanol do to Ca channels

what does this cause

A

inhibits Ca entry through voltage-gated Ca channels

-reduces NT release

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32
Q

what is the net effect of alcohol on neurons

A

neuronal inhibition (drowsy, anesthetic), shut down basic autonomic functions, death

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33
Q

does the alcohol dose that affects GABA affect dopamine release

A

yes DA is released at lower levels than GABA is activated

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34
Q

what is the controversy over delta subunits

A

they maybe delta subnuits dont play a role in sensitivity to low concentrations of ethanol, they dont know

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35
Q

what happens when you administer ethanol directly on the NAc

A

little if any dopamine release

still just tonic firing

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36
Q

what happens when you administer ethanol directly on the VTA

A
  • phasic firing, neurons depolarize with increased frequency

- increased DA release from VTA that synapse onto NAc

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37
Q

why do VTA DA neurons fire more often with ethanol when the rest of brain has decreased excitability (with ethanol present)

A

there are mu-opioid receptors on GABA releasing neurons which are activated by beta-endorphin which inhibit GABA release

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38
Q

what causes the release of beta-endorphin

A

ethanol

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39
Q

where does beta-endorphin bind (specific)

A

mu opioid agonist from projects that come from the hypothalamus

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40
Q

what happens when mu-opioid receptors are activated

A

inhibit voltage-gated calcium channel function, increase K+ channel function - causes hyperpolarization and decreased NT release

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41
Q

what is the effect of mu opioid receptor activation on GABA neurons

A

less GABA released

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42
Q

which part of the brain has mu receptors on GABA releasing neurons

A

VTA

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43
Q

what is the net effect when GABA is inhibited by mu opioid

A

glutamate still works, therefore excites DA releasing neurons in VTA

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44
Q

what happens do vessels with alcohol and how

A

vasodilation through central vasomotor control mechanism in brainstem

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45
Q

what happens to body heat with alcohol

A

feeling warm but core temp may decrease

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46
Q

what happens to digestive system with alcohol

A

may increase salivary and gastric secretion, hunger

but it eventually damages gastric mucosa - bleeding + irritation

47
Q

explain the pharmacodynamic tolerance for ethanol (3)

A 
downregulate GABA (an maybe changes subunit types to make less sensitive)
upregulate NMDA
upregular Ca channels
48
Q

what is behavioural tolerance

A

modify behaviours to mask effects of ethanol

49
Q

what is metabolic tolerance mainly with alcohol

A

upregulation of CYP2E1

50
Q

how much % does CYP2E1 metabolize in alcoholics

A

50-65%

51
Q

what else does CYP2E1 metabolize besides ethanol

and what does it turn them into

A

acetaminophen (tylenol), industrial solvents and some anesthetics into toxic metabolites

52
Q

are CYP2E1 levels variable in humans

A

yes, can have 8X variability

53
Q

what happens to CYP2E1 levels when volunteers were given 40g of ethanol a day for 5 week

A

some people had a large increase in CYP2E1 levels and some had a minimal increase

54
Q

what happens to ROS levels with CYP2E1 increase

A

they increase

55
Q

what happens with CYP2E1 knockouts in mice (what happens to liver)

A

they show less ethanol-induced liver damage

56
Q

what happens in mice with high CYP2E1 (what happens to liver)

A

they show more ethanol-induced liver damage

57
Q

what does upregulated CYP2E1 do to ROS

A

increases ROS in liver and other organs

58
Q

what is one of the major producers of ROS

A

up regulated CYP2E1

59
Q

what can ROS damage

A

DNA
lipids
proteins

60
Q

how does CYP2E1 metabolize ethanol into acetaldehyde (what does it use)

A

uses molecular oxygen to do it

61
Q

how can CYP2E1 produce ROS

A

as a byproduct if the reaction does not go to completion and oxygen does not get incorporated into the ethanol molecule

62
Q

what does a high level of ROS do to membrane

A

causes cell membrane damage which releases reactive lipid species from membrane -DNA damage

63
Q

how can chronic ethanol use cause cancer

A

high ethanol=high CYP2E1=high ROS =cell membrane damage=reactive lipid species from membrane=DNA damage=cancer

64
Q

how does body handle small amounts of ethanol that leads to ROS

A

small amounts can be more easily handled, we have many mechanisms to detox the ROS

65
Q

what are physical symptoms of hangovers

A 
headache
diarrhea
fatigue
tremulousness
nausea
66
Q

what are psychological symptoms of hangovers

A

decreased cognition, impaired visual spatial skills

67
Q

what BAC has symptoms peak

A

0%

68
Q

can cognition be impaired even though undetectable levels of ethanol in plasma

A

yes! studies show impaired functioning of pilots, drivers, skiers

69
Q

is dehydration the main cause of hangovers

A

no, rehydration only has a small effect on decreasing symptoms

70
Q

what do hangovers increase the production of

A

cytokines

71
Q

what does thromboxane B2 pathway do

A

produces cytokines

72
Q

what is likely the main cause of hangovers

A

increased cytokine production

73
Q

what is good evidence that hangovers could be caused by increased cytokine production

A

symptoms resemble viral infection & direct cytokine injection causes many hangover symptoms

74
Q

what is tolfenamic acid

A

a prostaglandin synthesis inhibitor

75
Q

what does tolfenamic acid do to hangovers and how

A

reduce symptoms by preventing cytokine production (prostaglandin synthesis inhibitor)

76
Q

what organelle is affected in hangovers and what happens and where

A

mitochondrial dysfunction in cerebellum

77
Q

what happens in cerebellum

A

integration of metabolic and sensory pathways

78
Q

what can mitochondrial dysfunction due to ethanol cause thats bad?

A

neuronal dysfunction or death

79
Q

what pathway does thromboxane b2 come from

A

prostaglandin synthesis

80
Q

what are congeners

A

toxic byproducts of alcohol production and storage

colors, flavours too

81
Q

what are examples of congeners (6)

A

acetone, methanol, acetaldehyde, tannins, furfural, fusel oil
colors, flavours too

82
Q

what color drinks tend to contain more congeners

A

dark

83
Q

how much more congeners are in bourbon than vodka

A

37X

84
Q

what does congeners do to hangovers

A

increased severity of hangover symptoms

85
Q

how many calories/gram in alcohol

A

7

86
Q

how many calories/gram in carbs

A

4

87
Q

how many calories/gram in protein

A

4

88
Q

how many calories/gram in fat

A

9

89
Q

what % of calories of average male canadian drinker comes from alcohol

A

13%

90
Q

what % of calories of average female canadian drinker comes from alcohol

A

8%

91
Q

what does the brain use as fuel in brains of heavy drinkers

A

switches from glucose to acetate during intoxication

92
Q

do alcoholics metabolize more or less glucose than non drinkers when intoxication

A

drinkers metabolize less ethanol

93
Q

what happens to NAD+ in ethanol metabolism and how

A

gets converted into NADH by alcohol dehydrogenase

94
Q

what does a high NADH:NAD+ ratio do to body fat metabolism

A

signals to synthesize fatty acids and stop fatty acid oxidation

95
Q

when does your body usually signal for fatty acid oxidation

A

when your body needs energy

96
Q

when does your body usually signal fatty acid synthesis

A

when you have lots of excess energy

97
Q

why does alcohol make a high NADH:NAD+ ratio

A

because there is an abundant energy source, so you store energy

98
Q

where does the synthesized fat go

A

stored as droplets in hepatocytes in liver

99
Q

what can happen when there is lots of fat in liver cells

A

they can cause cell lysis and inflammation

100
Q

is fatty liver reversible

A

yes if there isnt significant cell death

101
Q

what is fatty liver

A

high energy input from ethanol causes fat droplets to accumulate in adipocytes

102
Q

when does cirrhosis occur/for who does it occur

A

follows fatty liver if drinking continues

103
Q

is cirrhosis reversible

A

no

104
Q

what causes cirrhosis (general)

A

chronic inflammation and cell death

105
Q

what is TGF-beta

A

a transforming growth factor, a cytokine

106
Q

where does TGF-beta come from

A

liver cells

107
Q

what does TGF-beta do

A

binds to cell surface receptor of liver cells and stimulates intracellular pathways that affect gene transcription

-stimulates collagen synthesis

108
Q

what happens once cirrhosis progresses

A

functional liver cells are replaced by functioning connective tissue, mostly collagen
-cant detox blood as good

109
Q

what causes collagen synthesis in cirrhosis

A

TGF-beta binds to receptor and stimulates gene transcription

110
Q

what 2 compounds/molecules can modify lipids and proteins

A

ROS and acetaldehyde

111
Q

what does ROS and acetaldehyde do to lipids and proteins

A

modifies them so the body sees them as “foreign” - develops antibodies

112
Q

what causes the involvement of the immune system in alcoholic liver disease and inflammation

A

ROS and acetaldehyde modifies lipids and proteins them so the body sees them as “foreign” - develops antibodies

113
Q

how can ethanol cause inflammation

A

liver cells release cytokines that attract immune cells (binding to specific cytokine receptors on these cells)
also the antibodies due to ROS affecting lipids and proteins

114
Q

what do the activated immune cells do

A

infiltrate the liver, release ROS and RNS (reactive nitrogen species) + enzymes that destroy liver cells (usually kill pathogens)

PMCOL 305 (26 decks)

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