 Addiction  Chronic, relapsing disease characterized by a compulsion to seek and take drug,

loss of control in limiting intake

o Loss of control in limiting intake is the key aspect
o Point of addiction  loss of ability to control intake
 Emergance of negative emotional state
 Clinical perspective  DSM 4
o Undesired want to quit
o Substance use despite
 When does addiction occur?
o Whole life with no addiction
o Once and addiction occurs
 Cycle  spiriling cycle of distress
 These things must be there but not when it happened seeking and
attaining drug
o Binge intoxication  when drug is in use and effects present
o Withdrawal negative effect 
o Preoccupation anticipation  craving, larger amounts taken
than expected
o Acute effects are important but not why addiction occurs
 Mesolymbic dopamine  key pathway that causes addiction
 All of them activate this
 Craving stage  prefrontal cortex  long term good choices
 Disregulated with drugs of this area
o Become focused on getting something  short term
 Seeking drug > than life responsibility
o Drug cues  things that stimulate and use the hippocampus
 BLA in cues
 Nucleus Accumbens
 Extended Amygdala
 Medial Prefrontal Cortex
 Postive and negative reinforcement  presentation of a stimulus that cause increase in
response
o Drugs use positive reinforcement
 Activate mesolimbic dopamine system
 Uses dopamine
 Origine: VTA [Central tegmental area
 Extends through forebrain
 Synapses in the nucleus accombins
o Pleasure center for natural reinforcers
o Euphoria/pleasure increases activation of this pathway
 Lesion this pathway  drugs wont be used anymore
 Cocaine  most rewarding
o Normal functioning synapse  quick reuptake of dopamine
  Cocaine sits and blocks dopamine reuptake by sitting inside of dopamine
reuptake transporter
 Cocaine will quickly stimulate in development and maintence of drug
addiction
o 1 exposure of cocaine will increase tolerance
 Stimulant type of drug [like methamphetamine and Nicotine]
o Nicotine works on the cell body of VTA to cause release of
dopamine
 Cocaine cannot cause release of dopamine, just block reuptake
 Opiates  have shared effects  effect mew opiote receptors.
o Mew on interneurons  gaba neurons  blunt dopamine release
 Opiates will block the gaba neurons  less gaba  disinhibition
 Alcohol  small molecule
o Can modify all the receptors  doesn’t have binding site
o Wedge in between receptors  causes it to become more receptors
o Favorite targes  gaba and glutamate and some opiate
 Decreases gaba
 Increases glutamate
 Depressent
 Decreases fear and depression and anxiety
 Activates dopamine minimally
o Works primarily through negative reinforcement
 Alcohol doesn’t make people feel good
 Makes something bad go away [negative reinforcement]
 Removal of something bad causes increase of behavior
 Very effective anxiety go away
 Can make pain go away
 Alcohol and opiates
o Anxiolytic and analgesic  very effective coping strategy
 Brain compensates with alcohol to chronic exposure
 Pull away alcohol or opiates  begin cycle of distress
 Withdrawl syndroms
o Alcohol
 Physical symptoms
 Hyperexctied CNS
 Whole body temor
 Hyper irritability
 Rigidity
 Augmented susceptibility to siezures
 Deliurim tremens
 Typically lasts for 1-2 weeks
 Motivational (Affect) symptoms
 Anxiety, dysphoria, craving, can last for years
o Mostly responsible for relapse
 Type 1 achololics  turn to acholol to cope
 Test :
o VTA origin, end, dopamine
o Cocaine  dopamine transporters
o CRF in the central nucleus