Stimulant Use Disorders Flashcards
biological actions of stimulants (3)
- increases alertness and energy (elevating mood and appeal of drug-paired events)
- increases catecholamine transmission (DA, NE and Epi)
- binds catecholamine transporters to block uptake or reduce release
plant based stimulants (3)
- cocaine
- ephedra
- khat leaves
synthetic stimulants (5)
- amphetamine
- methamphetamine
- methylphenidate
- MDMA
- modafinil
transition to dependence is faster for who
faster in people with comorbidities (other SUDs, other psychiatric disorders)
internalizing vs externalizing disorders
internalizing -> difficulty regulating inwardly directed emotional turmoil (MDD, GAD, etc.)
externalizing -> difficulty regulating outwardly directed emotional turmoil (alcohol dependence, antisocial personality disorder, etc.)
why can’t addicted people stop consuming drugs (3)
- increased goal-directed approach (conditioned and sensitized incentive salience -> drug-related cues)
- development of compulsions (habits)
- switch from approach (use driven by reward) to avoidance (use driven by stress and withdrawal)
what are the triggers drug-seeking behavior (4)
- free shot of drug (stimulant drug-induced reinstatement)
- drug-paired cues
- stress
- withdrawal (if associations learned)
relationship between morphine and heroin
heroin is converted to morphine in the brain (but faster effect than morphine)
effect of drug-seeking behavior when (a) free shot of drug and (b) naltrexone-induced opiate withdrawal + conclusion
(a) very motivated to seek drug
(b) low motivation -> less likely to search for drug
conclusion -> withdrawal doesn’t induce drug-seeking behavior
what is needed for withdrawal to induce drug-seeking
learning the association that the drug relieves symptoms of withdrawal
effects of DA antagonist (haloperidol) on (a) PR breakpoint and (b) injection rate (cocaine self-administration) + explanation
(a) decreased motivation to seek drug
(b) increased # of injections/h
explanation -> if DA antagonist dilutes pleasure get from drug, less interested in getting the drug or inject more to get same amount as usual
effect of DA antagonist on (a) stimulant drug-induced reinstatement (b) cue-induced reinstatement (c) stress-induce reinstatement
(a) (b) decreased by DA antagonists
(c) decreased by NE antagonists
location of DA release in response to stimulants
ventral striatum (NAcc)
link between novelty seeking personalities and DA release
high novelty seeking personality -> more DA release (lower # of autoreceptors, greater DA release)
effect of inhibiting DA synthesis on pleasure when taking (a) cocaine (b) amphetamine (c) alcohol (d) tobacco + conclusion
pleasure of taking the drugs not altered -> DA not related to pleasure
effect of inhibiting DA synthesis on incentive salience/reward seeking of (a) cocaine self-administration and (b) alcohol rate of self-administration (c) alcohol PR breakpoint (d) cigarette PR breakpoint (e) money PR breakpoint
(a) disrupts ability to preferentially respond to reward-paired cues
(b) decreased alcohol ingestion
(c) decreased motivation to work for reward
(d) decreased motivation to work for reward (although dependent smokers worked harder than the others)
(e) decreased motivation to work for reward
conclusions on role of DA (3)
- pleasure is not required to change motivational states
- neurobiology is not the same (DA close to motivation, but not to pleasure)
- drug-seeking behavior is promoted by increased DA
effect of repeat amphetamine administration: DA sensitization (a) dose 1 (b) dose 4 (c) dose 5, 1 year later
(a) DA release in ventral striatum
(b) increased DA response
(c) effect still present and increased DA response; also DA release in dorsal striatum, linked with habit development
relationship between DRD2 # and cue-induced craving + DA release
low midbrain DRD2 = high drug cue-induced craving + high DA release
which relapse triggers induced DA release
all of them (low dose of drug, drug-paired cues, stress)
stress-induced DA release and maternal care
larger effects in people with low maternal care (more stress-induced DA release)
effect of naloxone-induced withdrawal on DA release
induces DA release in dorsal striatum (of people with opioid use disorder)
level of DA release in striatum of people with SUDs
most studies found low levels of DA release in response to a drug challenge in people with SUDs
DA response in caudate of addicted people vs control when expect to get drug and get drug
larger DA response in controls than addicted people (low DA release in addicted people)
DA response in caudate of addicted people vs control when don’t expect drug, but get it anyways
larger DA response in addicted people than control
what is the 3-factor model of addiction and psychiatric disorders
- externalizing personality traits
- early life adversity
- midbrain DA autoreceptors
what is the conclusion of the 3-factor model
3-factor model predicts common early onset DSM-V disorders
role of DA in individual bouts of drug/reward-seeking
increases in DA transmission promotes drug/reward-seeking (greater propensity to high DA states might increase risk for SUDs)
DA states following extensive substance use
alternation between high and low DA states
high DA state vs low DA state
high DA state -> promotes drug-seeking
low DA state -> aggravates withdrawal (increases contrast between abstinent and intoxicated states)
what should best treatments aim for
alleviate low DA state, redirecting reward-related processes to healthier pursuits (but too high dose of DA would promote drug-seeking behavior)
current best treatment for SUDs (3)
- contingency management therapy
- motivational therapy/CBT
- TSF (12 step facilitation)
off label medications for SUDs (3)
- methylphenidate
- modafinil
- SSRIs
experimental treatments for SUDs (6)
- ketamine
- N-acetyl-cysteine
- psychedelics
- OSU6162
- DBS
- TMS
