Alcohol Flashcards

1
Q

Mechanism of Action of alcohol

A
  • positive modulation of GABAA
    receptor function
  • negative modulation of AMPA and
    NMDA receptor function
  • general CNS depression
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2
Q

Mechanism of Action of alcohol ?

A
  • positive modulation of GABAA
    receptor function
  • negative modulation of AMPA and
    NMDA receptor function
  • general CNS depression
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3
Q

what is the effect of chronic alcohol exposure on the receptor function

A

Downregulation of GABA A receptor function

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4
Q

what is the mechanism of alcohol tolerance

A
  • subunit switch (e.g. 𝝰4)
    (cross-tolerance to other
    positive modulators)
  • increased internalization
  • altered phosphorylation
  • uncoupling of the GABA /
    ethanol sites
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5
Q

what are the ethanol receptors

A

Glycine receptor
BK channel

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6
Q

what are the alcohol withdrawal symptoms

A

minor withdrawal symptoms
seizures
delirium tremens
hallucination

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7
Q

what are the Pharmacological therapy for alcohol use disorder

A

Diazepam
Acamprosate
Naltrexone

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8
Q

how does Diazepam work

A
  • benzodiazepine that is used to treat anxiety and convulsions
  • approved for acute alcoholic withdrawal: symptomatic relief of acute
    agitation, tremor, and impending acute delerium tremens
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9
Q

how does Acamprosate work

A
  • dissociates into acetylhomotaurine and calcium
  • homologue of GABA
  • action not fully understood; restores the excitatory / inhibitory balance
    in the brain
  • indicated for maintenance of abstinence from alcohol
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10
Q

how does Naltrexone work

A
  • long-acting opioid receptor antagonist (𝝻,𝝹,𝝳)
  • action not fully understood; endogenous opioid system may be involved
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11
Q

how does

A

As an antagonist at the 𝝻 opioid receptor,
naltrexone may reduce the urge to consume
alcohol through two mechanisms:
* Suppression of alcohol-mediated
𝝱-endorphin stimulation of dopamine
neurons in the nucleus accumbens
* Reduction of 𝝱-endorphin disinhibition of
the tonic inhibition of dopamine cells by
GABAergic neurons in the ventral
tegmental area

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12
Q

How does Naltrexone reduce the urge to consume alcohol

A

As an antagonist at the 𝝻 opioid receptor,
naltrexone may reduce the urge to consume
alcohol through two mechanisms:
* Suppression of alcohol-mediated
𝝱-endorphin stimulation of dopamine
neurons in the nucleus accumbens
* Reduction of 𝝱-endorphin disinhibition of
the tonic inhibition of dopamine cells by
GABAergic neurons in the ventral
tegmental area

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13
Q

what is cannabis

A

delta9-tetrahydrocannabinol
(Ξ”9-THC)

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14
Q

how is the Ξ”9-THC concentrations in declining order:

A

flowering tops -> bracts -> leaves -> stems -> roots -> seeds

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15
Q

which cannabinoid is Psychoactive, Less Psychoactive, Not Really Psychoactive

A

Psychoactive (i.e., activation of CB1 receptors)
* Ξ”9-THC
Less Psychoactive
* Cannabichromene
Not Really Psychoactive (not active at CB1 or CB2 receptors)
* Cannabinol
* Cannibidiol

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16
Q

compare Pharmacokinetics of the cannabinoid

A

inhalation: Fast acting and early onset
- In blood within seconds
- 10-35% of THC in blood

ingestion;
- Slow acting and late onset
- Passes through the liver

17
Q

what are the behavioral effects of the cannabinoid

A

Subjects may have a form of disinhibition in that there is an inclination
to increase motor activity, and behavior is impulsive. However,
paradoxically, even the simplest tasks appear to require enormous
effort&raquo_space;»» Motor activity & impulsivity is up. Effort & coordination is down.

18
Q

what are the Problematic effects of Cannabinoid

A
  • Forgetfulness (working memory tasks)
  • Poor concentration
  • Motor coordination impairment
  • Poor sense of time
  • Reaction time slower
  • Some anxiety or paranoia
19
Q

what are the common withdrawal symptoms of cannabinoids

A

Common Symptoms
Decreased Appetite
Irritability
Nervousness/Anxiety
Anger
Restlessness
Sleep Difficulty/Strange Dreams

20
Q

how is the dopamine level after the THC withdrawal

A

Dopamine levels
are down during
withdrawal from
chronic THC

21
Q

what are the The β€˜endocannabinoids’

A
  1. Anandamide
  2. 2-arachidonyl glycerol (2-AG)
22
Q

How do Endocannabinoids work

A

Agonists at CB1 and CB2

23
Q

how does CB1 work

A
  • Expressed in the CNS (cerebral cortex, hippocampus, caudate putamen,
    basal ganglia, cerebellum)
  • Located on presynaptic terminals (thus, modulate neurotransmitter release)
24
Q

where does CB2 work

A
  • Very low expression
    in the CNS
  • Predominantly located
    in the periphery
25
what is Endocannabinoids: Mechanism of Action
Retrograde second messenger signalling to provide negative feedback
26
What are CB1 and CB2 receptors coupled with
Both CB1 and CB2 receptors are GPCRs that are coupled with Gi/o (inhibitory)
27
what is the signalling consequences of receptor activation
decreased function of adenylate cyclase - increased function of GIRK K + channels - decreased function of voltage-gated Ca2+ channels This all acts to hyperpolarize the local membrane potential and decrease neurotransmitter release
28
how annabinoids contribute to the reward pathway
Cannabinoids can activate the inhibitory CB1 receptor on GABAergic neurons to disinhibit the VTA dopaminergic neurons ---> increased DA release
29
what is the Acute THC reward pathway
- increased DA neuron firing in the VTA - increased DA release in the nucleus accumbens and prefrontal cortex (mesolimbic and mesocortical dopamine pathways) - increased content for tyrosine hydroxylase (DA synthesizing enzyme) - increased DA synthesis (CB1 receptor)
30
what is the Chronic THC reward pathway
- altered GLU and GABA signalling onto VTA DA neurons (below) - decreased DA synthesis and release in response to a rewarding stimulus - increased D2 receptor availability in postsynaptic neurons - morphological alterations to dendrites
31