alcohol Flashcards

harms associated with drugs, selected aspects of psychopharmacology of alcohol (ethanol), primary neuropharmacological targets of alcohol, psychological effects, alcohol-induced reduction in tension and anxiety, alcohol-induced memory loss ("amnesia"), mesocorticolimbic dopamine system and reward, chronic excessive alcohol use (38 cards)

1
Q

how was the drug harm scale developed?

A

experts assign score (0-3) for each parameter

parameters averaged to yield overall harm score

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2
Q

how was the criteria and rating improved?

A

16 criteria

scores from 0-100

differential weighting of criteria to indicate their different importance

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3
Q

what are the acute psychological effects of alcohol?

A

decreased tension/anxiety (anxiolysis)

impaired memory (amnesia, “black out”)

directly “rewarding” effects of alcohol

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4
Q

what are the psychological effects of chronic alcohol consumption?

A

neuropharmacological adaptions, withdrawal symptoms and alcohol dependence

severe and chronic cognitive deficits due to brain shrinkage (Wernicke-Korsakoff syndrome)

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5
Q

what are the non-specific pharmacological effects of alcohol?

A

interactions with lipid bilayer

mainly at higher concentrations - not really relevant when we drink alcohol unless very excessive

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6
Q

what are the specific neuropharmacological effects of alcohol?

A

interactions with ligand-gated ion channels (i.e. neurotransmitter receptors) and voltage-gated ion channels

at concentrations within range achieved by common alcohol consumptions

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7
Q

what is the first hit of alcohol?

A

neurotransmitter receptors (NMDA, GABA-A, 5-HT23, nACh)

voltage-gated ion channels (L-type Ca2+ channels, GIRKs)

leading to cascade of synaptic events involving many neurotransmitters

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8
Q

what does acute alcohol do overall?

A

tends to dampen neural activity

e.g. stimulation of inhibitory GABA receptors

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9
Q

what do the psychological effects of alcohol depend on?

A

complex interactions between many variables

environmental variables (social cues)

cognitive set (expectancy)

mood, arousal, personality factors

age and sex of subjects

exposure to other drugs (coffee, nicotine, etc) and nutritional state of subjects

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10
Q

what are the variables related to ethanol ingestion?

A

dose

rate of ingestion

time of testing post ingestion, time of day

type of beverage ingested (role of congeners)

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11
Q

what happens as you drink more alochol?

A

blind alcohol concentration increases

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12
Q

what has been shown about the relationship between alcohol and a reduction in tension and anxiety?

A

studies on human subjects reported variable effects on measures of anxiety

similar to classical anxiolytics, alcohol acts as indirect agonist at GABA-A receptors

comorbidity of anxiety disorders and alcohol abuse

alcohol relatively consistently reduces measures of anxiety in rodents

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13
Q

what is that cat odour avoidance test?

A

put cat odour in rat’s cage and rats have innate anxiety of cats - don’t approach

when anxiety reduced, might come out

rats who had high alcoholic beer, hid less and approached cat odour

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14
Q

what was the elevated plus maze test?

A

rats don’t like open high spaces so wouldn’t exposure elevated maze

high alcohol = high time spent outside

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15
Q

what was the test of ethanol self-administration in rats?

A

split into high and low anxious rats

option to give themselves ethanol

high administering in low anxious than high anxious rats

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16
Q

what memory does alcohol interfere with?

A

especially with encoding of new information into long term declarative memory

17
Q

what is declarative memory?

A

memory that can be consciously recalled consisting of events

18
Q

what is alcohol-induced anterograde amnesia?

A

range from little memory lapses to “fragmentary” to “en block black outs”

19
Q

what are “en block black outs”?

A

partial or complete absence of memory

particularly when large amounts

20
Q

what was Aaron White et al’s (2002) study into alcohol-induced memory loss?

A

asked undergraduates

“have you ever awoken after a night of drink not able to remember things that you did or places that you went?”

51% of those who have ever consumed alcohol answered “yes”

21
Q

what are the possible mechanisms of alcohol-induced memory loss?

A

state dependence

selective interference with hippocampal memory mechanisms

22
Q

what is state dependence?

A

information encoded/learnt in drug state may be remembered better if tested in comparable drugged state rather than non-drugged state

need to be in similar state as when learning/encoding to retrieve optimally

alcohol shown to render some aspects of declarative memory state dependent

evidence for asymmetric state dependence - retrieval especially reduced in AS but less so in SA group

however appears to account mainly for little memory lapses or fragmentary blackouts - en block blackouts seem to be due to other mechanisms

23
Q

how is state dependence normally tested?

A

experiments usually include 4 groups in 2x2 design

AA = alcohol, alcohol

AS = alcohol, sober

SS = sober, sober

SA = sober, alcohol

two independent variables = state when encoding, state when retrieving

24
Q

what is the state dependence word association test?

A

learning phase (day 1) = subjects asked to respond to 10 words with the first word that comes to mind

recall phase (day 2) = subjects cued with the words and asked to recall their response from day 1

recall better in group AA than in AS - state dependency

25
what is selective interference with hippocampal memory mechanisms?
mainly interferes with encoding of new declarative information interference with hippocampal synaptic mechanism of memory disrupts induction of hippocampal long term potentiation
26
how does alcohol disrupt induction of hippocampal long term potentiation?
activity-dependent long-lasting increase in synaptic strength and a candidate physiological mechanism of memory under baseline condition, glutamate ion only activate AMPA magnesium blocking NMDA receptors if very intense stimulation of post-synaptic terminal then depolarised and magnesium block expelled so NMDA receptor can contribute to transmission - allow for calcium ions in and results in intracellular cascades - make synapse stronger
27
what are animal studies into selective interference with hippocampal memory mechanisms?
when mimic learning experience, responses in hippocampus increase and stay high when go back to baseline if inject with alcohol, long term differentiation goes
28
what is the mesocorticolimbic dopamine system?
drive our reward system within brain - makes use want things more reward motivates us to keep going dopamine system = reward system dopamine mainly produced in midbrain regions which projects to much of frontal and accumbens rewards activate mesocorticolimbic dopamine transmission
29
how can intracerebral microdialysis be used to measure neurotransmitters?
put microdialysis probe into brain region of interest then flush artificial CSF past membrane then collect and analyse contents of extracellular space go into fluid depending on concentration of neurotransmitters
30
what did intracellular microdialysis find?
all drugs massively increase dopamine transmission experience is very rewarding hijack natural reward system by stimulating it
31
what are the neuropharmacological adaptions to repeated and chronic alcohol use?
contribute to dependence long-term compensatory changes in neural mechanisms which are opposed to acute effects of alcohol contributing to tolerance (reduced acute alcohol effects) and chronic psychological changes when sober (withdrawal)
32
what is withdrawal hyperexcitability?
altered balances between excitatory and inhibitory neurotransmission in response to chronic alcohol possible effects - withdrawal symptoms (seizures, tremor, withdrawal anxiety, alcohol craving) and excitotoxic brain damage (if neurons get excited too strongly, get killed, resulting in long term cognitive deficits)
33
what does reduced dopamine transmission during withdrawal mean?
reduced nucleus accumbens dopamine during withdrawal dopaminergic neurons fire less in withdrawal period possible effects - reduced sensitivity to (natural) rewards and reduced motivation
34
how has reduced nucleus accumbens dopamine during withdrawal been tested?
inject with alcohol - rats dopamine transmission goes up after, level go below control level - withdrawal period
35
what is Wernicke-Korsakoff syndrome?
caused by thiamine deficiency most commonly in association with alcoholism Wernicke syndrome Korsakoff amnesia
36
what is Wernicke's syndrome?
acute stage characterised by ophthalmoplegia (paralysis of eye muscles), confusion, ataxia
37
what is Korsakoff amnesia?
remains after treatment of acute Wernicke syndrome if thiamine deficiency lasted too long global impairment in forming new declarative memory severe brain "shrinkage" especially in striking degeneration of mammillary bodies
38
are there cognitive deficits and brain shrinkage in "uncomplicated" alcoholics?
uncomplicated = without Wernicke-Korsakoff syndrome may present with deficits in sensori-motor and executive function, learning and memory may show marked fronto-cerebeller brain damage