alcohol Flashcards
how are the harms associated with drugs assessed - old version
- physical harm and dependence to users
- social harms to others
- experts assign score 0-3 for each parameter
what is the improved criteria for harms associated with drugs
- 16 criteria
- scores from 0-100
- differential weighting of criteria to indicate their different importance
why is it suggested that alcohol is the most harmful over other drugs
- a combination of an expert assessment of drug harm to users and to others
what are the acute psychological effects of alcohol
- decreased tension/anxiety
- impaired memory
- directly rewarding effects of alcohol
what are the psychological effects of chronic alcohol consumption
- neuropharmacological adaptations, withdrawal symptoms and alcohol dependence
- severe and chronic cognitive deficits due to brain shrinkage - wernicke-korsafokk syndrome
what are the nonspecific effect of alcohol
- interactions with lipid bilayer, mainly at higher concentrations
what are specific effects of alcohol
- interaction with ligand-gated ion channels and voltage-gated ion channels, at concentrations within range achieved by common alcohol consumption
what is the first hit of alcohol process
- first hit is inhibitory activity - dampens down neural activity in the brain
- neurotransmitter receptors
- voltage-gated ion channels
- then a cascade of synaptic events involving many neurotransmitters
what is the primary neuropharmacological targets of alcohol process
1- alters lipid composition
2- interacts with polar heads of phospholipids
3- disturbs the relationship of protein in membrane
4- acts at neurotransmitter binding site
5- modifies gating mechanism inside channel
6- direct interaction with channel protein
7- stimulates G which is linked to adenylyl cyclase
what variables effect the psychological effects of alcohol in humans
- environmental variables
- cognitive set
- mood, arousal and personality factors
- age and sex of subjects
- exposure to other drugs
- nutritional state of subjects
- the dose
- rate of ingestion
- time of testing post ingestion
- type of beverage ingested
what alcohol concentration is lethal
0.45
what is the legal driving limit of alcohol in the UK
between 0.06 and 0.08
how does alcohol reduce tension and anxiety
- alcohol acts as indirect agonist at GABA-A receptors i.e. enhances the response of the major inhibitory neurotransmitter GABA
what did Kushner et al 2000 find about anxiety and alcohol
- commorbidity
what did blanchard et al find about anxiety and alcohol
- alcohol relatively consistently reduces measure of anxiety in rodents
what beer drinking and anxiety researched
- cat odour avoidance test
- elevated plus maze test
how does alcohol interfere with memory
- declarative memory
- alcohol induced anterograde amnesia may range from little memory lapses to ‘fragmentary’ or ‘black outs’
what did Aaron White et al find about alcohol induced memory loss
- asked undergraduates ‘ have you ever woken after a night out and not remembered’
- 51% said yes
how is alcohol induced amnesia explained by state-dependence
- info encoded in a drugged state, may be remembered better if tested in a comparable drugged state
- overton
what is the word association test to check state dependent effect of alcohol
- learning phrase - subjects respond to 10 words with the first word that comes to mind
- recall phase - subjects cued with the words and asked to recall their response from day 1
which group in the word association task had the biggest difference
- biggest difference between those who learned and recalled under alcohol and those who learned with alcohol and recalled sober
what does state dependency explain and not explain according to Goodwin
- explains little memory lapses and fragmentary blackouts
- doesn’t explain en block blackouts
what might contribute to alcohol induced amnesia
- interference with hippocampal synaptic mechanisms of memory may contribute
what did Bliss and Collingridge find alcohol disrupts
the induction of hippocampal long-term potentiation
what is hippocampal long-term potentiation
- an activity-dependent long-lasting increase in synaptic strength and a candidate physiological mechanism of memory
what is the basic process of LTP
- baseline - NMDA receptor is blocked by magnesium
- intense stimulation - NMDA receptor can start contributing - lets calcium ions in which increase efficiency of AMPA receptors - making it more sensitive and increases number which makes the synapse stronger
- AMPA receptors chemically modify so that each receptor allows more current through leading to a larger excitatory post synaptic potential
what affect does alcohol have on postsynaptic response
- long lasting increase - LPT is affected by alcohol consumption
what can alcohol effect and cause problems for
- general disorientation
- sexual activity
- violence
- disciplinary action
- personal injury
- school performance
how does alcohol interact with our dopamine system
- alcohol drives our reward system and makes us want things
where is the dopamine system located
- produced in midbrain region which projects the forebrain
what do rewards activate
the meso-corticolimbic dopamine transmission
what are the features of the meso-corticolimbic dopamine system
- nucl. accumb. - has D1 and D2 receptors where rewards are involved
- ventral tegmental area - involves rewards
how does the meso-corticolimbic dopamine system cause addiction to alcohol
- the final pathway for rewards - reduces activity on neurons which leads to disinhibition of GABA receptors in the VTA which leads to an increase in dopamine
what is intracerebral microdialysis
- measures neurotransmitters
- measures extra cellular space in the brain and measures the dopamine concentration in a particular brain region
how do neuropharmacological adaptations to repeated and chronic use of alcohol contribute to dependence
- leads to long term compensatory changes in neural mechanisms in response to chronic excessive alcohol, which are opposed to acute effects of alcohol - maintains equilibrium
- leads to tolerance in response to repeated alcohol use - GABA receptors might need more alcohol
- leads to chronic psychological changes when sober - anxious and more excitable
what is withdrawal hyperexcitability
- altered balance between excitatory and inhibitory transmission in response to chronic alcohol
what happens where there is altered balance between excitatory and inhibitory neurotransmission in response to chronic alcohol
- decreased GABA-A receptor function - compensating for acute GABA enhancing effects of acute alcohol
- increased glutamate receptor stimulation and function - compensating for decreased glutamate release and decreased NMDA receptor function in response to acute alcohol
what are the possible effects of withdrawal hyperexcitability
- many withdrawal symptoms - seizures, tremor, withdrawal anxiety, alcohol craving
- excitotoxic brain damage - long term cognitive deficits - neurons are excited so strongly that they get killed
what happens during withdrawal
reduced dopamine transmission
- reduced nucleus accumbens dopamine during withdrawal
- reduced spontaneous activity of dopaminergic neurons in the VTA
what is a possible effect of reduced dopamine transmission during withdrawal
- reduced sensitivity to rewards and reduced motivation
what is Wernicke-Korsakoff syndrome
- caused by thiamine deficiency, most commonly associated with alcoholism
- involves wernicke syndrome and korsakoff amnesia
what is wernicke syndrome
- acute stage, characterised by ophtalmoplegia, confusion and ataxia
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
