Barker lecture 4 Flashcards
Schedule 1
No medical use, high abuse potential
Heroin, marijuana, THC, LSD
Schedule 2
Medical use, HIGH ABUSE, large risk for dependence
Morphine, fentanyl, cocaine, PCP
Schedule 3
Medical use, moderate abuse
Ketamine, buprenorphine, Marinol (THC in oil capsule)
Schedule 4
Medical use, low abuse
Benzodiazepine
Schedule 5
lower risk relative to IV
cough suppressants with small amount of codeine
Opioids
GPCR
heroin, prescription meds
mu
LSD, mushrooms
psilocybin, psilocin
5-HT2A/C
Marijuana, K2, spice
Cannabinoid receptors CB1
Gamma hydroxy butyric acid
GABAb
Caffeine
adenosine receptors
Cocaine, amphetamine
DAT
MDMA/ecstacy
monoamine transporters
dopamine, serotonin
Alcohol
GABA channels, 5HT3, NMDAR, nAchR, KiR3
causes release of endogenous opioids
Nicotine
act on ion channels
ionotropic acetylcholine receptors
agonist
PCP, Ketamine
ion channels
Ionotropic NMDA receptor
Antagonist
Benzodiazepines, barbiturates
ion channels
Ionotropic GABAa receptors (Cl-)
Positive allosteric modulators
Role of dopamine in pathway of addiction
Decision making impulsivity: frontal cortex
Pleasure valuation: nucleus accumbens
Source of dopamine: VTA
Reward/value: striatum/SN
Memory learning: hippocampus
STIMULANTS, DEPRESSANT AND PSYCHEDELICS ALL ACT ON THE MESOLIMBIC SYSTEM
STIMULANTS, DEPRESSANT AND PSYCHEDELICS ALL ACT ON THE MESOLIMBIC SYSTEM
The dopamine hypothesis of addiction
“Pleasurable events” release dopamine
Parkinson patients only develop addiction during treatment
Dopamine important for assigning value to reward prediction error
Value provides the drug with an incentive salience
Salience= state or quality of an item that stands out to relative to neighboring items
Limits of the dopamine hypothesis
Dopamine does not encode liking, but involved in making reward predictions and learning from the outcome/error
The glutamate hypothesis of addiction
Glutamate can increase dopamine activity in NAcc
Glutamate projection to VTA
Destruction of this pathway reduces cocaine/morphine reward
NMDA antagonist blocks acquisition of reinforcement learning
Intra NAcc AMPA injection causes relapse
Dopamine controls glutamate activity in amygdala
Drug use induces long term changes in neuronal plasticity
LTP=long term potentiation
“persistent increase in synaptic strength following intense stimulation”
Rewarding substances cause relative increase in glutamatergic AMPA receptors
DSM-5 SUD criteria
Mild (2-3)
Moderate (4-5)
Severe (>6)
Physical dependence
Body needs more drug–>tolerance
Body withdraws without drug
Emotional withdrawal symptoms
Anxiety, depression
Restlessness, insomnia
Irritability
Headaches
Poor concentration
Physical withdrawal symptoms
Sweating
Racing heart
Goosebumps=cold turkey
Muscle spasms=kicking the habit
Tremors
Nausea, vomiting, diarrhea
Dangerous withdrawal symptoms
Alcohol and tranquilizers
Grand mal seizures (also tramadol)
Heart attacks, stokes
Hallucination, delirium tremens (DT)
Physiological dependence
addiction
mental urge to take drug to function
compulsive need/craving
even in absence of withdrawal
Positive reinforcement
Drug is “rewarding” or produces positive reinforcement when the user feels pleasure/satisfaction
Of value, strengthen behavior to repeat
Just liking isn’t enough
Negative reinforcement
reward by escaping negative/painful stimulus or event (NOT same as punishment)
Stimulants
cocaine
amphetamine
meth
bath salts
ecstasy
nicotine
Depressents
opioids
alcohol
cannabis
GHB
inhalants
Psychedelics
LSD
Psilocybin
PCP
Mescaline
Ketamine
