drugs and addiction lect 3 Flashcards

1
Q

learning theory and addiction

A

-dominant approach
-explores drug and non drug addictions
-behaviour as a result of reinforcement and punishment
-antecedents may make sensitisation to reinforcement from substances more likely in some people e.g genetic markers or trauma

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2
Q

pos reinforcement

A

-drug using behaviour, often the effects, are pos reinforcing in early episodes
-this is the liking stage
-other reinforcement may come from social acceptance/bonding

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3
Q

what is contiguity

A

how clearly the behaviour and effect are linked in time
(pos reinforcement needs to occur as soon as poss for behaviour to be reinforced, some ROA are faster and these tend to be more addictive)

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4
Q

classical cond and repeated drug use

A

-frequent drug use can lead to cues in the environment strongly associated with the drug use e.g certain people, places etc
-initial exposure
NS (environmental stim associated with drug) - UCS (drug effects on brain) - UCR (reactions to drug, brain prepares)

-subsequent reactions
CS (environmental stim associated) - CR (compensatory reactions to drug, brain prepares)

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5
Q

pos reinforcement and neural systems

A

-drugs release DA in mesolimbic and mesocortical DA systems from the VTA
-nucleus accumbens plays important role
(-induces humans/animals to seek/ consume drugs
-animals will work hard for drug reward, especially psychostimulants
-cues associated with drugs will trigger drug seeking in humans and animals)

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6
Q

neg reinforcement

A

-use of drug can remove unpleasant stim
-substances may be used to reduce pain or psychological discomfort
-with repeated use, removal of withdrawal is motivation
-contiguity: how soon you feel effects = more reinforcing
-often pathway of addiction is from pos reinforcement to neg reinforcement
–initial stage: drug for pos effects
–later: drug for removal of withdrawal
-increasing use separates liking and wanting
-wanting relates more to neg reinforcement

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7
Q

tiffany CC

A

drug related stim can induce cravings

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8
Q

Robins CC

A

US soldiers dependent on heroin in vietnam but rarely continued to use at home (they were out of the environment so had no cues)

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9
Q

wickler

A

-opioid withdrawal in group therapy with now drug free clients, when talking about the drug they started sniffing and yawning showing signs of withdrawal

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10
Q

conditioned place preference

A

-place initially NS
-repeated drug use in same place means this place becomes CS

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11
Q

siegal place preference

A

-gave rats large doses of heroin
-control (not addicted) were 95% likely to die
-rats who had been cond to be addicted to heroin were less likely to die
-when given dose in same environment as when addiction was cond, the rats were less likley to die

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12
Q

cond tolerance

A

Ehrman
-opioid detoxed pp given signalled or unsignalled (whether they knew it was coming) dose of hydromorphone or placebo
-greater physiological approach to drug when unsignalled

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13
Q

needle freaking

A

Levine
-heroin users when heroin not available
-go through ritual of preparing to inject but use saline or something else instead
-mild high, some physiological signs and some withdrawal reversal seen

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14
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A
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15
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16
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18
Q

addiction therapy based on CC

A

cue exposure therapy: aims to reduce cond drug effects
-based on idea of extinction, repeated non reinforced exposure to drug cues diminishes cond drug effects
(research inconclusive)

18
Q

-what are the main gateway drugs

A

alcohol, nicotine, cannabis

18
Q

gateway hypoth of drug use

A

-use of psychoactive drug increases probability of further drug use
-first time use of specific drugs is not random but shows trends
-use of drugs often in sequence
-other variables effecting drug use: age, gender, family, laws, mental health etc

19
Q

what are the drug reward pathways in the brain

A

-both pathways are involved in rewarding properties of the drug
-mesolimbic pathway originates in VTA and terminates in nucleus accumbens, amygdala and hippocampus
-mesocortical pathway originates in VTA and terminates in frontal cortex
(activated by drug and non drug rewards)

20
Q

DA hypoth

A

-original hypoth: addictive drugs release dop but non addictive drugs do not
-da release in mesolimbic and mesocortical pathway is increasingly rewarding and this action is addictive
-da findings indicate da release in certain drugs either directly or indirectly but not in others that are not addictive

21
Q

reward prediction error (RPE)

A

diff between received and predicted rewards
-if we regularly receive a reinforcer, subjective reward can diminish (habituation)
-cond cues lead us to expect reward, reward is less than expected (rpe)
-dopamine activity presented when there is an error between reward expectant and received

22
Q

RPE and cocaine

A

-cocaine dependent users vs non users
-dopamine signals of reward expectation similar for both groups
-signal for received reward was lower for cocaine dependent users in ventral striatum and orbitofrontal cortex bc cocaine dependent users expected the reward

23
Q

role of da in reward (pleasure)

A

-olds and milner: rats repeatedly self stimulate certain brain areas with electric impulses (pos reinforcement)
–these brain areas shown to be made up heavily of da neurons
–drugs like cocaine directly increase da and increase self stimulation of these areas

-blum et al: da could be released by addictive drugs
–using drugs which block da receptors can impair reinforcements gained from psychostimulant drugs in rats and primates

-larnelle: in humans, increase in da in striatum correlates with euphoria produced by stimulants

24
Q

weaknesses of da hypoth

A

-if drugs are effective due to da then medications altering da should be able to treat addiction? despite research to find a medication for addiction, nothing has transpired
-studies with alcohol, ketamine and cannabis have failed to show changes to da release
-blocking da receptors in rats failed to reduce rewarding actions of opiates
-leyton: depiction of da before cocaine use in experienced users had no effect on euphoria experienced by drug

25
Q

what does this leave us with regarding the da hypoth

A

-we expect da involvement in highs from dependent psychostimulant use as stimulants act on da receptors
-da must be the mediator - if psychostimulants release da then it must be involved in the high
-however this is correlational not causal
-other drugs that effect da indirectly dont show the same relationship with da release and drug high
-da definitely has a role and may be involved in motivation to use drugs
-role of da and addiction is unclear
-likely to be numerous neurotransmitter systems involved in drug use and addiction

26
Q

incentive sensitisation theory

A

Robinson and berridge
-drug wanting and liking are separate
-wanting outlines withdrawal, neg reinforcement cannot account for all relapses
-as drugs are wanted more and more, liking decreases

27
Q

how does incentive sensitisation work

A

addictive drugs share ability to enhance certain dopamine pathways
-da systems attribute incentive salience to stim associated with activation of the system (rendering them wanted)
-da systems make sure we pay attention to certain stim e.g drugs and sugar, they are rewarding so we repeat use
-in some indiv, repeated use of addictive drugs changes system making it more hypersensitive to drugs and associated stim
-drug wanting can continue for a long time after liking has decreased and after drug use has ceased

28
Q

support for incentive theory

A

-lambert: discrepancy between liking and wanting cocaine in LT heavy dependent users
-amphetamine sensitisation increased incentive salience attributed to CS (sucrose associated lever) even when rats were tested drug free - Wyvell and berridge
-ostafin: measured wanting vs liking in relation to alcohol, wanting predicted risky drinking better than liking
-kiyatkin: da increased in anticipation of heroin self administration in rats who had had heroin before, da decreased once drug administered, supports incentive salience

29
Q

da and incentive sensitisation theory

A

-critical da pathways that undergo neuroadaptation for addiction render these brain systems sensitised to drug and associated stim
-da systems that are sensitised DO NOT mediate the pleasurable or euphoric effects of drugs (liking) but an element of reward: incentive salience (wanting)
-role of da related directly to reinforcement BUT not necessarily to pleasure and euphoria (RPE)

30
Q

evidence for role of da in reward not pleasure

A

martinez
-pp with addictions had lower no of da receptors in striatum months after ceasing drug use
-brain has been sensitised to drug use with downregulation of da receptors
-removal of drug leaves blunting of da (shortage) due to downregulation of da receptors
-this may be why substance is still wanted months after

31
Q

Blum et al 2015

A

-reviewed 3 suggestions about role of da in drug use and addiction: liking, learning and wanting
-argues that Nutt is too quick to dismiss the evidence that da has a role to play in compulsive use aside from use of psychostimulants
-they show there does seem to be involvement of da in the mediation of reward from other drugs of abuse NOT just psychostimulants as Nutt suggested

32
Q

da and compulsive drug use summary

A

-da does play role in reinforcing properties of drugs, separate to the hedonic effects
-da deficiency may be involved in drug seeking in people with biological susceptabilities
-using drugs may sensitise da pathways to encourage seeking further highs
-link to RPE: drug use maintained, reward diminishes but expectation of reward remains
-precise mechanism behind drug seeking is still being explored
-da interacts with other neurotransmitter activity and systems

33
Q

what is GABA

A

a system da interacts with
-Nutt and Nester
-major inhibitory neurotransmitter
-drugs can down or upregulate GABA system
-involved in modulating reward and reinforcement
-GABA implicated directly in drug action from use of alcohol, ketamine etc
-has inhibitory role in other systems like da
-can be effected by other systems e.g opioid neural system can effect GABA functioning

34
Q

what does evidence of GABA suggest

A

GABA system disturbances (lack of typical GABA activity) might pre date substance misuse
-GABA implicated in medications to treat addiction

35
Q

glutamate

A

Nutt and Nestor
-major excitatory neurotrans. in brain
-repeated substance use thought to involve process of pathological changes in brain
-e.g plasticity of da responding due to learning and reward in midbrain striatum
-glutamate interacts with other neurotransmitters
-also involved in memory and learning and development of addiction

36
Q
A