Who becomes addicted: genes, stress and dopamine receptors
Explains why some people use drugs without developing addiction while others do: genetics (including opioid and dopamine receptor differences), chronic stress, comorbid mental illness and social context.
Where this fitsConnects to 2 · Unlocks 2
- Connects to
- The course lens: biopsychosocial, and no 'chemical imbalance' — This is the biopsychosocial lens applied to addiction.
- Dose-response curves: potency, efficacy, slope and variability — Receptor density differences are one source of variability.
- Unlocks
- From use to addiction: receptor loss, hypofrontality, craving and relapse — Low receptor density can be a cause — or a consequence — of heavy use.
- Treating addiction: substitution, antagonists, glutamate, vaccines — and the model's limits — Genetic differences can predict who a treatment helps (naltrexone and alcohol).
Orient
Individual differences in addiction likelihood: genetic differences, stress (especially chronic stress), comorbid mental illness and social contexts. Two genetic examples from class: the alcohol and mu-opioid receptor polymorphism, and the density of DA receptors in the nucleus accumbens.
Course terms
Your professor's wording, word for word from the slides. Learn the term and this definition — the explanation underneath is only there to help it make sense.
- Individual differences
“Genetic differences Stress (especially chronic stress) Comorbid mental illness Social contexts”Slides 06, p. 6
Why some people use without becoming addicted.
- Mu-opioid receptor polymorphism
“Alcohol and mu-opioid receptor polymorphism (Ray et al., 2012)”Slides 06, p. 6
If alcohol agonizes mu-opioid receptors in a person, drinking is more “pleasurable” and addiction more likely.
- DA receptor density
“Density of DA receptors in nucleus accumbens”Slides 06, p. 6
Non-users with fewer DA receptors rated methylphenidate “more pleasurable” (Volkow et al., 2004).
From your course: Course slides 06, pp. 16–18
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