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Dynamics of neuronal circuits in addiction: Reward, antireward, and emotional memory

Academic Article
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Overview

authors

  • Koob, George

publication date

  • 2009

journal

  • Pharmacopsychiatry  Journal

abstract

  • Drug addiction is conceptualized as chronic, relapsing compulsive use of drugs with significant dysregulation of brain hedonic systems. Compulsive drug use is accompanied by decreased function of brain substrates for drug positive reinforcement and recruitment of brain substrates mediating the negative reinforcement of motivational withdrawal. The neural substrates for motivational withdrawal ("dark side" of addiction) involve recruitment of elements of the extended amygdala and the brain stress systems, including corticotropin-releasing factor and norepinephrine. These changes, combined with decreased reward function, are hypothesized to persist in the form of an allostatic state that forms a powerful motivational background for relapse. Relapse also involves a key role for the basolateral amygdala in mediating the motivational effects of stimuli previously paired with drug seeking and drug motivational withdrawal. The basolateral amygdala has a key role in mediating emotional memories in general. The hypothesis argued here is that brain stress systems activated by the motivational consequences of drug withdrawal can not only form the basis for negative reinforcement that drives drug seeking, but also potentiate associative mechanisms that perpetuate the emotional state and help drive the allostatic state of addiction.

subject areas

  • Allostasis
  • Animals
  • Fear
  • Humans
  • Illicit Drugs
  • Memory
  • Neural Pathways
  • Pain
  • Reinforcement (Psychology)
  • Reward
  • Substance Withdrawal Syndrome
  • Substance-Related Disorders
  • Systems Biology
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Identity

PubMed Central ID

  • PMC2739305

International Standard Serial Number (ISSN)

  • 0176-3679

Digital Object Identifier (DOI)

  • 10.1055/s-0029-1216356

PubMed ID

  • 19434554
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Additional Document Info

start page

  • S32

end page

  • S41

volume

  • 42

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