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Molecular Neuroscience III > 3 - Alcohol Abuse > Flashcards

3 - Alcohol Abuse Flashcards

1
Q

When does alcohol have the strongest effect on the developing brain?

A

The first month of pregnancy and embryonic stage

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2
Q

What is a toxic metabolite from ethanol?

A

Formaldehyde

Can be prevented by alcohol dehydrogenase, which will convert it to acetaldehyde

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3
Q

What enzyme in the brain produces reactive oxygen species in response of ethanol? What is another enzyme in the brain for alcohol metabolism?

A

CYP2EI

Catalase produces acetaldehyde (AA), which is responsible for the majority of damage observed in neurons

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4
Q

What process in the brain leads to DNA damage?

A

Folate mediated one-carbon metabolism

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5
Q

What NT receptors does alcohol effect?

A
  • stimulates GABAa receptors
  • sensitization of NMDA receptors
  • D1 receptors associated with alcohol reward
  • D2 receptors involved as well (how?)
  • μ (decrease EtOH), κ (decrease EtOH), δ (increase etOH) opioid receptors affect alcohol consumption
  • Neuropeptide Y decreases EtOH intake when overexpressed and increases it when aberrant
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6
Q

How does alcohol affect protein kinase C-y and protein kinase C-ε?

A

PKCy: Critical enzyme for addiction

PKCε: alcohol sensitivity (upregulation with chronic alcohol and increased sensitivity)

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7
Q

What type of genes in the brain are associated with alcohol-dependence?

A

Enzymes that degrade alcohol

  • Alcohol dehydrogenase
  • Acetaldehyde dehydrogenase
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8
Q

How id dopamine and cAMP regulated neuronal phosphoprotein (DARPP-32) affected by alcohol?

A

When DARPP is knocked out, mice have less preference for sweet saccharin and alcohol, but not for food and water.

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9
Q

What do inhibitors of opioid receptors (for cancer treatment) sometimes cause as a side effect?

A

Increased alcohol consumption

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10
Q

What type of receptor is decreased by drug abuse? What is the likely consequence of this?

A

Dopamine D2 receptor in striatum

This probably explains tolerance

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11
Q

What does exposure of alcohol cause physiologically in the gross anatomy/functioning of the brain?

A
  • Swelling of ventricles

- Deficit in brain activity at cortical areas and cerebellum

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12
Q

Alcohol causes neuroinflammation. How?

A
  • Alcohol simply comprises blood-brain barrier function and allows leukocytes to enter, inducing neuroinflammatory cascade
  • Direct interaction of alcohol on Toll like receptors (TLRs) on astrocytes and glia, especially TLR4
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13
Q

What does knockout of toll like receptor 4 (TLR4) show?

A

No neuroinflammation from astrocytes and microglia in chronic alcohol exposed brains

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14
Q

What does neuropeptide Y (NPY) do for control of alcohol?

A
  • Interaction with GABAergic system
  • NPY2 receptors activated postsynaptically on GABA neurons
  • Stimulation of GABAergic neurons via CRF in amygdala is counteracted by NPY to counteract the enzyme induced by CRF
  • NPY is involved in eating behaviour, so not a good target in treatment of alcohol abuse
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15
Q

What is the consequence of MALAT-1 upregulation in the brain from alcohol abuse?

A
  • Non-typical alternative splicing

- MALAT is an important factor in the action of alcohol and can cause neuronal cell death

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16
Q

Where is MALAT one overexpressed from dosing alcohol? What is the consequence of this?

A
  • Upregulation in cortex during withdrawal

Alternative splicing of proteins involved in alcohol mediation can cause alcohol-induced excitotoxicity (posibly from overexpression of NMDA synapses) and memory impairment

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17
Q

What is the role of histamine and serotonin in alcohol abuse?

A

Histamine and 5-HT seem to be regulators that counteract alcohol intake.

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18
Q

What pathway is histaminergic transmission most likely working on during alcohol abuse?

A

Mesolimbic reward pathway

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19
Q

What do antagonist of 5-HT reuptake transporters do for alcohol abuse?

A
  • Reducing alcohol uptake in type A alcoholics (less severe, later onset), but not in type B
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20
Q

Why can energy drinks be hazardous to mix with EtOH?

A

Caffeine inhibits effects of alcohol, needing a higher dose for intoxication.

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21
Q

Why is illicit drug use an infrequent cause of death compared to legal drugs like tobacco and alcohol?

A

An illicit drugs use is much less common compared to legal use of alcohol and tobacco and therefore it is also a scarce cause of death. Tobacco smoking results in more than 5 million deaths each year and accounts for almost 90% of all deaths from lung cancer whereas deaths caused by alcohol abuse are estimated as over 2 millions per year.

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22
Q

True or false? Majority of people who drink alcohol control the amount imbibed.

A

True

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23
Q

How much alcohol a day is considered harmless and some studies even show beneficial effects of alcohol consumed in small amounts on the overall health?

A

Two drinks a day (28 gram pure alcohol) for mean and 1 drink (14 gram pure alcohol) for women.

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24
Q

How many drinks over a 2 h period are considered as harmful or binge drinking.

A

Five drinks for mean

Four drinks for women

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25
Q

How many times is alcohol abuse as common in men as it is in women?

A

Two times as common in men

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26
Q

What are fetal alcohol spectrum disorders (FASDs) caused by?

A

Maternal alcohol consumption during pregnancy

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27
Q

What are fetal alcohol spectrum disorders characterized by?

A
  • pre- and postnatal growth deficiencies,
  • craniofacial anomalies
  • CNS dysfunction.

CNS abnormalities observed in FASD include:

  • microencephaly,
  • abnormal cortical thickness,
  • reduced cerebral white matter volume,
  • ventriculomegaly
  • cerebellar hypoplasia.
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28
Q

Binge drinking that produces high
blood alcohol levels (BAL≥ 200 mg/dL), is more damaging to the fetus than chronic alcohol exposure that produces lower BALs (≤ 150 mg/dL). What are some other factors that contribute to severe FASDs?

A
  • Facial dysmorphology, a feature of FAS, appears to arise only when high-peak BALs occur during the embryonic stage of gastrulation. Depending on the time and levels of alcohol exposure, alcohol may affect the molecular mechanisms that include: alterations in gene expression, interference with the mechanisms of neural stem cell proliferation, migration, differentiation, cell-cell interactions, cell survival, oxidative stress and glia activation.
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29
Q

Name five alcohol induced pathologies

A
  • Can damage developing PFC and hippocampus
  • Neuropathies from multiple vitamin B deficiencies
  • Anterior lobe cerebellar degenerative disease and Wernicke-Korsakoff syndrome (resulting from thiamine deficiency and characterized by sever short-term memory loss)
  • Global brain atrophy in severe drinkers.
  • Higher risk of head and neck cancers, stomach cancer, liver cancer and breast cancer.
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30
Q

Name two mice and two rats that are selected for different alcohol preferences

A

Mice:

  • alcohol preferring: C57BL/6
  • alcohol avoiding: DBA/2

Rats:

  • alcohol preferring: AA, P
  • alcohol avoiding: ANA, NP
31
Q

List the steps of alcohol metabolism

A
  • Ethanol, alcohol dehydrogenase converts to:
  • Acetaldehyde, acetaldehyde dehydrogenase converts to:
  • Acetate
32
Q

Where is the majority of alcohol metabolized?

A

Liver

33
Q

An average 70 kg person oxidizes ___ of pure ethanol per hour

A

10 ml of pure alcohol per hour

34
Q

How can alcohol metabolism in the brain cause DNA damage?

A

There is no alcohol dehydrogenase in the brain, but instead alcohol can be metabolized by catalase (accounts for 60–70% of ethanol-generated acetaldehyde in the brain) and cytochrome P450 2E1 (CYP2E1), which accounts for 10–20%.

Both reactive oxygen species (ROS) produced by CYP2E1 and acetaldehyde can induce DNA damage.

35
Q

Which two enzymes can metabolize alcohol in the brain?

A
  • Catalase

- Cytochrome P450 2E1 (CYP2E1)

36
Q

Describe folate-mediated one-carbon metabolism of alcohol. What can indicate dysfunction of this important biochemical pathway?

A

One of a major biochemical processes altered in chronic alcohol abuse is one-carbon metabolism. Tetrahydrofolate (THF) polyglutamates are a family of cofactors that carry and chemically activate one-carbon units for biosynthesis.

Important step in this process is methionine recycling via methylation of homocysteine. The elevated homocysteine levels were observed in patients with chronic alcoholism, which may indicate dysfunction of this important biochemical pathway.

37
Q

“broadly,” how does alcohol affect the brain?

A

In the past alcohol effects was believed to act by perturbing the lipid membrane. Alcohol facilitates GABAA and glycine transmission and inhibits NMDA- mediated glutamatergic transmission.

38
Q

What is evidence for GABAa as a mediator of alcohol effects?

A

GABAa, glycine induction – Mutation of a single amino acid in specific transmembrane domains (TM2 and TM3) of the α2 and β subunits of GABAA and glycine (TM2) receptors abolish the action of ethanol. Mutations of γ subunit seem to be less important.

39
Q

How is protein kinase C involved in the effects of alcohol?

A
  • PKCγ null mutant mice displayed reduced sensitivity to the effects of ethanol.
  • PKCε knockout mice are supersensitive to alcohol; acute low dose of ethanol and other drugs such as diazepam and pentobarbital, which activate GABAA receptors have hyperlocomotor and high-dose sedative effects. In addition, these mice voluntarily consume 75% less alcohol than wild-type mice when tested by using a two-bottle choice paradigm. Chronic ethanol treatment induces PKC upregulation. Interestingly PKCε knockout mice also self- administer less nicotine and have reduced place preference for nicotine.
40
Q

How is NMDA signalling altered by alcohol? (3)

A

Mechanism unclear.

  • Numbers of both the NMDA- Rs and the voltage-dependent Ca2+ channels are increased after chronic ethanol.
  • There is observed up-regulation of NMDAR1–1 and down-regulation of the NMDAR-2B subunit both at the mRNA and protein levels.
  • AMPA receptors and the kainate receptors are unaltered after 16 days of ethanol exposure.
41
Q

What enzymatic deficiency causes someone to be more susceptible to alcohol?

A

Human ALDH22 and ADH22 (acetaldehyde and alcohol dehydrogenases alleles) lead to the accumulation of alcohol’s metabolite, acetaldehyde, when a person drinks alcohol. This toxic compound produces nausea, flushing, dizziness, and other unpleasant effects, and slow alcohol metabolizers avoid excessive drinking.

42
Q

Mice lacking functional D1 receptors showed what in terms of alcohol intake?

A
  • Mice lacking functional D1 receptors drank less ethanol and showed lower preference across a range of concentrations compared to heterozygous and wild- type littermate control mice in both limited and continuous-access two-bottle procedures.
  • D1 knockout mice also drank less ethanol (12%) when it was the only fluid available for 24 h.
  • Selegiline (10 mg/kg), an MAOB inhibitor that increases synaptic DA levels, reduced ethanol intake in wild-type and heterozygous mice, but had no effect on D1 knockout mice.
  • Similarly, treatment with a D1 receptor antagonist (SCH-23390, 1 mg/kg) reduced ethanol intake in wild-type and heterozygous mice, but not in D1 knockout mice.
43
Q

What does injection of a D2 receptor antagonist do to ethanol intake?

A
  • Injection of a D2 receptor antagonist (sulpiride, 50 mg/kg) nearly eliminated the already low ethanol intakes of D1 knockout mice.
  • D2 knockout mice drank less ethanol but also responded less for water, food, and saccharin, suggesting a relatively broad, nonspecific impairment of motivated responding.
44
Q

How is DARPP-32 an alcohol response gene?

A

DARPP-32 (dopamine- and cAMP-regulated neuronal phosphoprotein) null mutants showed lower responding for ethanol and saccharin, but not for food or water in a continuous access operant self-administration procedure.

45
Q

What happens to ethanol intake when μ-opioid receptors are knocked out? κ-opioid receptor KO? δ-opioid receptor KO?

A

μ KO: Reduced alcohol intake
κ KO: Increased alcohol consumption
δ KO: Greater preference for ethanol

46
Q

What do β-endorphin deficient mice show in terms of ethanol intake?

A

Greater self administration of ethanol

Chronic free choice ethanol consumption causes increased β-endorphin immunoreactivity in the hypothalamus and septum of alcohol-preferring mice (C57BL/6), and Met-enkephalin expression in the nucleus accumbens of ethanol-preferring AA rats

47
Q

What does disruption of the NPY gene cause for ethanol intake?

A

Disruption of the NPY gene increases ethanol intake, whereas over-expression of the NPY gene reduces ethanol intake in a homecage two-bottle procedure.

48
Q

What does genetic/pharmacological blockade of CB1 receptors cause for alcohol intake?

A

In mice genetic deletion and pharmacological blockade of cannabinoid CB1 receptors reduces alcohol intake. The inhibition of cannabinoid uptake in mice stimulates alcohol consumption.

49
Q

What happens to dopamine D2 receptor density in drug abusers?

A

In people addicted to various drugs and alcohol it is observed that there is a general tendency of decrease of the striatal brain D2 receptors. This may explain development of tolerance to the drugs.

50
Q

How does alcohol drinking induce changes in brain morphology and activity? (3)

A
  • Increased brain ventricle volume (reverse slowly in sobriety)
  • Higher activity in dorsolateral prefrontal and parietal cortex compared to alcoholic brain
  • In alcoholics, increased activity is observed in a fronto–parieto–cerebellar network probably to compensate deficit in the other areas.
51
Q

How does alcohol cause neuroinflammation? (2)

A
  • Disruption of blood–brain barrier (BBB) by alcohol promotes leukocyte migration, which may induce neuroinflammatory processes.
  • Alcohol can also directly activate the toll-like receptors (TLRs) in astrocytes and microglia, which results in downstream stimulation of nuclear factor-κB (NF-κB) and the induction of genes that encode inflammation-associated molecules and cytokines.
52
Q

What kind of mice KO can protect against both the activation of microglial and astroglial cells and the production of cytokines and inflammatory mediators, in brain injury induced by long-term alcohol consumption?

A

As an effect buildup of damage-associated molecular
patterns (DAMPs), including cellular debris, which are a ligands of TLRs leads to amplification of inflammatory process. Mice knockout of TLR4 protects against both the activation of microglia and astroglial cells and the production of cytokines and inflammatory mediators, in brain injury induced by long-term alcohol consumption.

53
Q

Describe alcohol-induced neurotoxicity in C57BL/6 alcohol preferring mice given a 3 week alcohol containing diet (5)

A
  • Significant increase in TUNEL/MAP-2 staining in cortical slices indicated rise of apoptotic signaling in the brain neurons. MAP-2 is a neuronal marker (microtubule-associated protein 2).
  • After 3 weeks the markers of ROS- induced DNA modifications (oxo8dG) and acetaldehyde-derived N2-ethyl-dG were significantly increased.
  • Short (4 days) ethanol exposure induced DNA repair which was significantly lower after 3 weeks of ethanol consumption. Parallel to these changes was observed ethanol exposure-dependent increase in aldehyde-derived N2-ethyl-dG.
  • Folate-dependent one-carbon metabolism is necessary to re-metylate of homocysteine to methionine. 3-week but not 4-day exposure to ethanol increases blood homocysteine with parallel observed decrease of methylation processes in the brain.
  • Heterozygous MTHFR mice (methylenetetrahydrofolate reductase - catalizes methylation of homocysteine), show potentiated response to ethanol. The same mice have reduced ability to self- repair DNA.
54
Q

How does NPY counteract the action of ethanol in amygdala GABAergic neurons? How might it be used to treat alcohol addiction? (4) What is a disadvantage of this method? (1)

A

Alcohol stimulates GABA release.

  • Neuropeptide Y (NPY) microinjection into the amygdala was able to suppress alcohol drinking in rats trained to self administer alcohol.
  • This treatment also reduced withdrawal effects probably by reducing anxiety.
  • NPY injection to amygdala blocked CRF-induced increases in anxiety-like behavior.
  • Neuropeptide Y may suppress alcohol drinking in rats via tonic activation of presynaptic Y2Rs in amygdala, and this effect may be buffered by NPY actions at postsynaptic Y1Rs in the same region. This raise the possibility to use novel NPY ligands that cross blood-brain barrier in the therapy of alcoholism.
  • The disadvantage of this method could be appetite-stimulating effect of NPY.
55
Q

What is MALAT-1?

A

A non protein-coding RNA upregulated in the brain of alcoholics

  • MALAT-1, (also known as NEAT2) belongs to group of nuclear-retained regulatory RNAs (nrRNAs), which was shown to modulate alternative splicing (AS) of pre-mRNA by interacting with serine/arginine (SR) splicing factors
  • Increase of MALAT-1 transcripts was detected in cerebellum, hippocampus and brain stem, of human alcoholics. GAPDH is glyceraldehyde 3-phosphate dehydrogenase expression used for comparison.
    -
56
Q

What does deletion of MALAT-1 in vitro lead to?

A

Depletion of MALAT-1 in vitro leads to aberrant mitosis which manifest in fragmented nuclei in the post-mitotic cells. Observed is also strong increase of cell death in the MALAT-1 deficient cells.

57
Q

When is MALAT-1 most upregulated in the rat cortex?

A

During withdrawal.

58
Q

How is dopamine sensitivity modulated by ethanol to lead to increased alcohol preference? (1) How is this seen in the glutamatergic system? (2)

A
  • Ethanol is known to affect alternative splicing of dopamine D2 receptor pre- mRNA, which may lead to increased alcohol preference by modulating dopamine sensitivity.
  • The alternative splicing of NMDA receptor may contribute to alcohol- induced excitotoxicity and memory impairment.
  • MALAT-1 was shown to increase expression of genes involved in synapse formation which may contribute to the NMDA-induced excitotocity.
59
Q

How does alcohol alter histamine and its H1 and H3 receptor in rats? What pathway does this involve?

A
  • There were observed lower histamine H1 and H3 receptor levels in cortex, septum and nucleus accumbens of alcohol-preferring AA rats. H3 receptor antagonists decrease alcohol self administration in AA rats.
  • Histamine was increased by 120% in the hypothalamus and by 170% in the septum in AA rats. Significantly higher histamine concentration was also found in the frontal cortex (60%) and hippocampus (90%) of AA rats.
  • Most probably the histamine effects on alcohol consumption involves its interaction with mesolimbic dopamine pathway.
60
Q

How can serotonergic agents be used as a treatment for alcohol abuse? How does its effects differ for type A alcoholics and type B alcoholics? (3)

A
  • Serotonin uptake antagonists can reduce alcohol uptake in type A alcoholics (type A have less severe substance dependence, later onset of addiction and less comorbid psychological dysfunction whereas type B alcoholics have earlier onset, a greater amount of stress, more childhood environmental risk factors, history of polydrug abuse, potential for comorbid psychological dysfunction, and greater severity of dependence).
  • 5-HT3 antagonist, ondansetron was found to be effective in type B alcoholics but not in type A.
  • 5-HT1a receptor agonist, buspirone, shows potential to reduce symptoms of alcohol withdrawal.
61
Q

What does KO of the adenosine transporter (ENT1) cause with alcohol intake? How does caffeine affect this?

A

ENT1 (adenosine transporter) mice knock-out exhibits increased alcohol preference and drink voluntarily more alcohol.

Caffeine, an adenosine antagonists, counteracts behavioral effects of ethanol.

ENT1-deficient mice also show reduced GLT1/EAAT2 (glutamate transporter) expression in glia.

62
Q

How can an antibiotic of the glutamatergic system be used to reduce alcohol consumption?

A

Antibiotic ceftriaxone, which increases expression of GLT1 in glia was able to reduce alcohol consumption in alcohol- preferring rats with history of long-term heavy consumption of ethanol.

63
Q

How is the adenosine transporter (ENT1) on astrocytes involved in ethanol-induced EAAT2 expression? How did ENT1 KD effect this?

A

In cultured astrocytes, an ENT1-specific antagonist and siRNA treatments significantly reduced both EAAT2 expression and glutamate uptake activity while ENT1 overexpression up-regulated EAAT2 mRNA expression. The ethanol exposure caused:
- Increased EAAT2 mRNA expression as well as glutamate uptake activity

  • ENT1 knockdown inhibited the ethanol-induced EAAT2 up-regulation.I
64
Q

Acute alcohol induces adenosine activation of A1 receptors, which are known to inhibit ___?

What are consequences of this?

A

Acute alcohol induces adenosine activation of A1 receptors (A1R) which are known to inhibit the wake-promoting neurons of the basal forebrain (BF) to promote sleep.

  • Chronic alcohol reduces adenosine levels inducing insomnia.
  • Acute alcohol decreases, whereas chronic alcohol increases, the glutamatergic transmission.
65
Q

Acute alcohol ___ glutamatergic transmission.

Chronic alcohol ___ glutamatergic transmission.

A

Acute alcohol decreases glutamatergic transmission.

Chronic alcohol increases glutamatergic transmission.

66
Q

What biomarkers can be used to quantify chronic alcohol abuse? non protein (3) and protein (2)

A

Non-protein biomarkers

  • Mean corpuscular volume (MCV), erythrocyte size
  • Ethyl glucuronide [EtG]
  • 5-hydroxy-tryptophol [5-HTOL]

Protein biomarkers

  • Carbohydrate-deficient transferrin [CDT]
  • γ-glutamyl transferase (GGT)
67
Q

True or false? There is no available method that is 100% accurate in detecting chronic alcohol abuse. Errors are frequent.

A

True

68
Q

What is disulfiram (calcium carbimide)?

A

It blocks acetaldehyde metabolism to treat alcoholism – produces nausea, dizziness, and other unpleasant effects when drinking.

69
Q

What is Naltrexone?

A

An opioid antagonist, decreases pleasurable effects of alcohol

70
Q

What is acamprosate?

A

Glutamate antagonist – reduces the incidence of alcoholism relapse

71
Q

What is topiramate?

A

Antagonizes glutamate and dopamine, enhances GABA – anticonvulsant

Alcohol treatment

72
Q

What is the relapse rate for alcoholism after treatment?

A

Treatment not very successful.

At 3 months post- treatment 40–60% of individuals relapse to a
first drink. By 12 months this rate increases to 70–80%.

73
Q

Describe chronic alcohol abuse and cancer. Which mutation is most associated with this? What is the major carcinogen involved?

A
  • Some malignant tumours of the oral cavity, pharynx, larynx, oesophagus, liver, colorectum and female breast are related to the consumption of alcoholic beverages.
  • Similar effect were observed in laboratory animals chronically treated with alcohol.
  • People with mutation of alcohol dehydrogenase and acetaldehyde dehydro- genase are in a high-risk group to develop cancer.
  • The major carcinogen involved is acetaldehyde, a product of alcohol metabolism. In laboratory animals inhalation of acetaldehyde induced various carcinomas. Acetaldehyde interferes with DNA synthesis and repair. Alcohol dehydrogenase can be also involved in metabolism of estrogens. This could be a risk factor in developing breast cancer. It is estimated that about 5.2% in men and 1.7% in women of all cancers is a result of chronic alcohol consumption.
  • A consumption of more than 80 g alcohol a day (approximately a 0.7 litre bottle of wine) is associated with an 18-fold higher head and neck cancer risk whereas smoking 20 cigarettes a day increases the risk by 5-fold only. Smoking and drinking have synergistic effect on cancer.

Molecular Neuroscience III (8 decks)

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