How does gender affect risk of drug addiction?
- dependent on drug, but usually men
- but gap is closing: from 5-1 to 3-1 (men-women)
- women - “telescoping”: when addicted to drugs, progress thru stages of drug use faster than men
How does age affect risk of drug addiction?
- often begins in adolescence: extended exposure to drug
- but “telescoping”
How does depression & anxiety affect risk of drug addiction?
both causes & effects of addiction
How does ethnicity & genetics affect risk of drug addiction?
- evidence for predisposition to addiction: e.g. genes for alcohol metabolism, family clusters
- no single gene for addiction/particular addiction
- troubles w/ implicit bias in society/researchers
How does environment affect risk of drug addiction?
- family history: exposed to drug use as socially normal, more likely to use that drug
- poverty: more likely to find ppl w/ addiction problems
- chronic stress
- early childhood adversity
What causes drug addiction?
changes in structure & function of brain:
- drugs of abuse act on brain - alter motivation, leads to increased drug-seeking behaviour - addiction is not "failure of willpower"
What are the stages of drug addiction?
- intoxication
- development of dependence
- preoccupation & anticipation
What are the features of drug addiction? Which is the most important feature?
- pleasing effects
- craving
- tolerance
- escalation of intake
- dependence
- relapse
- continued use despite adverse effects on life (most important)
What is the caffeine example of the opponent process theory of addiction? (baseline)
Example of tolerance: caffeine
baseline conditions: adenosine builds up thruout day & binds to adenosine receptors, causing us to feel sleepy
What is the caffeine example of the opponent process theory of addiction? (new)
new coffee drinker:
- caffeine: adenosine antagonist, blocks adenosine receptors
- prevents adenosine from binding & signal no longer transmitted
- cells deprived of adenosine signals, realise smth gone wrong & adapt to changes
What is the caffeine example of the opponent process theory of addiction? (chronic)
chronic coffee drinker: additional adenosine receptors added
- overcome effects of caffeine
- same amount of adenosine binding to receptors, feel just as sleepy before drinking coffee
- drink more coffee, then more adenosine receptors added (repeats)
What is the caffeine example of the opponent process theory of addiction? (chronic skips)
chronic coffee drinker who skips morning coffee:
- same amount of adenosine & way more adenosine receptors w/ no caffeine
- many adenosine binding to receptors
- exaggerated effect of adenosine: feel extra sleepy, headache
- withdrawal symptoms
What features does the opponent process theory of addiction explain? Why is it generally considered insufficient to understand addiction?
- ppl go back to using drug even after withdrawal symptoms have disappeared
- explains some drug taking behaviours
- but cannot explain relapse & why drugs w/ little withdrawal are so intensely motivating
Is dopamine the pleasure molecule?
no
- all addictive drugs directly/indirectly increase dopamine transmission
- all increase dopamine function but not all feel pleasurable
- can be intensely motivated to do smth but not necessarily for pleasure
What is evidence for dopamine not being the pleasure molecule? (SNc)
- substantia nigra pars compacta (SNc): other main dopamine producing area in brain
- Parkinson’s patients:
- lost SNc
- dopamine levels change
What is evidence for dopamine not being the pleasure molecule? (L-DOPA)
- crosses BBB & enzymes in brain convert L-DOPA into dopamine
- Parkinson’s patients:
- restore motor functions
- no change in baseline levels of pleasure
What is evidence for dopamine not being the pleasure molecule? (schizophrenia)
Schizophrenia patients:
- hyperactivity of dopamine
- don’t have higher baseline pleasure
What is evidence for dopamine not being the pleasure molecule? (Salomone)
Salomone:
- pleasure & motivation separable things, effects of dopamine due to motivation not pleasure
- dopamine receptor antagonists:
- decrease motivation but not pleasure - choose low effort, low reward option
What does dopamine do?
- some stimuli have innate/learned incentives
- incentives facilitate DA release onto NAcc: teaching signals, motivational signals, other functions
- NAcc gets many inputs, guide behaviour (valuation)
What is the incentive sensitization theory (dopamine theory of addiction)? What features does it explain? Why is it generally considered a more comprehensive theory of addiction?
- separates liking (pleasure) vs. wanting (motivation)
- all addictive drugs increase DA
- drug use adds incentive salience to drug stimuli:
- artificially increase DA levels
- sight of drug cues facilitates motivation
- explains important elements that withdrawal theory cannot
What is treatment for addiction?
psychological & pharmacological therapies:
- detoxification (rehab)
- drug replacement therapy: take dangerous drug & replace w/ safer alternative
- behavioural therapy
- cognitive behavioural therapy
- twelve-step programs
Why is treatment generally very unsuccessful?
- drug addiction changes structure & function of brain itself:
- long term changes depending on usage
- changes seen in areas VTA targets: frontal cortex, nucleus accumbens, hippocampus
- focused on notion that if you can get thru withdrawal, you can be clean: drug taking not driven primarily by withdrawal
How can we treat/cure drug addiction?
- have individuals avoid cues associated w/ drug
- successful treatment for addiction requires large changes in social, economic & mental health conditions
What does the dopamine theory of addiction suggest about recovery from addiction?
- drug taking driven by change in motivational system: artificial increase in DA levels
- main problems driving addiction itself not solved: poverty, stress
- participants left in feedforward mechanism:
- increased impulsivity, decreased behavioural flexibility
- makes them more predisposed to problems w/ addiction in future
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(2) neuropsychopharmacology basics20
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(3) brain basics26
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(4) neural communication I26
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(5) neural communication II & drug properties (midterm 1)14
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(5) neural communication II & drug properties (midterm 2)28
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(6) addiction26
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(7) psychostimulants37
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Previous Lectures4
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(8) nicotine & caffeine36
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(9) alcohol34
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(10) opioids24
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(11) cannabis22
