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Addiction Model
Thought of as a cycle with 3 stages: the 3-stage model
Preoccupation with anticipation stage
preoccupation with obtaining the drug, persistent physiological problems, the idea of taking the drug becomes stronger
Binge Intoxication Stage
Escalated drug usage/frequent intoxication
stems from a persistent desire for the drug, typically resulting in larger doses of drug
Withdrawal Negative Affect Stage
Stopping the drug, but experiencing negative side affects as a result of abstinence, tolerance, compromised social/occupational/recreational activities, ect
consists of bad mood, physical pain, enhanced desire for drug, ect
Reward Citcuit
Pathway in the brain that mediates the acute rewarding and reinforcing effects of most recreational drugs
Mesolimbic DA Pathway
VTA to the Nucleus Accumbens, almost all drugs activate this pathway either by enhancing VTA firing or increasing extracellular DA levels in Nacc
Abused Drugs Firing?
Mimics burst firing
DA receptors
D2 has a higher affinity for DA; therefore only elevated levels will activate D1
D1 is more important for reward than D2, but both play a role in addiction
Incentive Sensitization Theory of Addiction
the distinction between liking versus wanting a reward (the incentive)
Incentive Salience
having the desire to take the drug when in the presence of strong stimuli, despite not wanting the drug
Psychostimulants & Dopamine
DA is necessary for the rewarding effects of psychostimulants
Other drugs and Dopamine
DA is a contributing factor to reward, but not required
Reward-Prediction Error
DA signal the difference between prediction of receiving a reward and actual occurrence of reward
Kyperkatifeia
Negative emotional state evoked by drug withdrawal, proposed to be a core feature of addictive disorders
Within-System Adaptations
results in progressive down regulation of activity
Natural reward is harder to satisfy
Between System Adaptations
Gradual recruitment of antireward system (amygdala)
put a limit or break on reward
Activates aversive effects like stress, sadness, pain, ect
Brain Images of Addiction
Shrinks w/ addiction
Dysfunctions in PPFC plays into drug craving, leads to intrusive thinking of drug
Insula implicated with motivational regulation
Thalamus relays drug-induced stimuli to insula
Cue-Induced craving
correlates paired stimulus (drug) with activation of PFC
Behavioral Control Brain Areas
Shifts from striatal areas (pleasure related) to habitual areas (habit)
Ventral striatum to dorsal striatum
“Go” System
motivates and activates learned responses
Inital drug use to addiction invokes an enhancement of the GO system; tunrs from goal directed to behavioral habit
“Stop” System
system that stops the habit
dysfunction of this system, which includes to PFC components
Leads to intrusive thinking, drug craving, and loss of impulse control
Recovery
Varies in individuals, random cravings can return due to long-lasting changes in the brain that alter gene expression/changes in synaptic plasticity/reward/antireward
Desensitized Gene
expression changes via methylation
Chronic use results in the gene desensitized.
Repressed Gene
Acetylation or Phosphorylation leads to chromatin opening “primed” genes for expression
With too much drug, the gene for specific pathways can be reperssed
Synaptic Plasticity
After 1 exposure of a drug, the brain was changed and maintained it for 5 days
Disease (medical) model
views addiction as a disease, based on evidence for dysregulation of brain function
Moral Model
Addiction was seen as a sign of personal and moral weaknesses
Criticisms of Disease Model
Brain alteration does not prove addiction as a disease
No single diagnostic test to confirm the disorder
empirical evidence raises doubt that heavy drug usage is outside of users control
Non Disease Theories
Argues that addicts choose the drug because it serves a purpose; alleviating pain, lack of positive reinforcement, provides motivation
Contingency Management
Rewarded when tox screen is negative