Addiction: a disease of learning and memory.

  title={Addiction: a disease of learning and memory.},
  author={Steven E. Hyman},
  journal={The American journal of psychiatry},
  volume={162 8},
  • S. Hyman
  • Published 1 August 2005
  • Psychology, Biology
  • The American journal of psychiatry
If neurobiology is ultimately to contribute to the development of successful treatments for drug addiction, researchers must discover the molecular mechanisms by which drug-seeking behaviors are consolidated into compulsive use, the mechanisms that underlie the long persistence of relapse risk, and the mechanisms by which drug-associated cues come to control behavior. Evidence at the molecular, cellular, systems, behavioral, and computational levels of analysis is converging to suggest the view… 

Neural mechanisms of addiction: the role of reward-related learning and memory.

Progress in identifying candidate mechanisms of addiction is reviewed, including molecular and cellular mechanisms that underlie long-term associative memories in several forebrain circuits (involving the ventral and dorsal striatum and prefrontal cortex) that receive input from midbrain dopamine neurons.

New approach to the neurobiological mechanisms of addiction.

  • Z. FürstP. RibaM. Al-Khrasani
  • Biology, Psychology
    Neuropsychopharmacologia Hungarica : a Magyar Pszichofarmakologiai Egyesulet lapja = official journal of the Hungarian Association of Psychopharmacology
  • 2013
The aim of this review is to collect and interpret the latest opinions in the development, the underlying mechanisms and therapy of addiction as a disease of central nervous system.

The synaptic pathology of drug addiction.

This chapter discusses the current understanding of drug-induced neuroplasticity within the mesocorticolimbic brain system that contributes to the development of addiction and the persistence of relapse to drug seeking.

Targeting drug memory reconsolidation: a neural analysis.

Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

A greater understanding of the neurobiological mechanisms involved in the extinction of drug-related memories could provide novel therapeutic interventions for the treatment of drug addiction.

Neuroplasticity in addiction: cellular and transcriptional perspectives

A summary of more recent research that has furthered understanding of drug-induced neuroplastic changes both at the level of the synapse, and on a transcriptional level, and how these changes may relate to the human disease of addiction is provided.

New approaches to addiction treatment based on learning and memory.

These approaches suggest that the extinction of drug-related memories may represent a viable treatment strategy in the future treatment of addiction.

Drug addiction: An affective-cognitive disorder in need of a cure

Addiction and Cognition

  • T. Gould
  • Psychology, Biology
    Addiction science & clinical practice
  • 2010
The brain regions and neural processes that underlie addiction overlap extensively with those that support cognitive functions, including learning, memory, and reasoning, and the adverse impact on cognition may be particularly deleterious in combination with cognitive problems related to their mental disorders.



Molecular Neurobiology of Drug Addiction

  • E. Nestler
  • Biology, Psychology
  • 1994
The purpose of this review is to illustrate the ways in which molecular neurobiological investigations will contribute to an improved understanding of drug addiction and, ultimately, to the

Drug abuse: hedonic homeostatic dysregulation.

This framework provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and to relapse in individuals with a history of addiction.

Addiction and the brain: The neurobiology of compulsion and its persistence

Evidence is reviewed for the possibility that compulsion and its persistence are based on a pathological usurpation of molecular mechanisms that are normally involved in memory, which is often initiated by exposure to drug-related cues.

Limbic-Striatal Memory Systems and Drug Addiction

Drug addiction can be understood as a pathological subversion of normal brain learning and memory processes strengthened by the motivational impact of drug-associated stimuli, leading to the

Common Molecular and Cellular Substrates of Addiction and Memory

  • E. Nestler
  • Biology, Psychology
    Neurobiology of Learning and Memory
  • 2002
A better understanding of the molecular and cellular adaptations that occur in these neural circuits may lead to novel interventions to improve memory and combat addiction in humans.

Learning mechanisms in addiction: synaptic plasticity in the ventral tegmental area as a result of exposure to drugs of abuse.

  • J. Kauer
  • Biology, Psychology
    Annual review of physiology
  • 2004
This review focuses on alterations in cellular and synaptic physiology in the ventral tegmental area (VTA) in response to addictive drugs.

Addiction as a Computational Process Gone Awry

A computational model of addiction is constructed that over-selects actions leading to drug receipt and provides an explanation for important aspects of the addiction literature and provides a theoretic view-point with which to address other aspects.

Addiction, a disease of compulsion and drive: involvement of the orbitofrontal cortex.

It is implied that pleasure per se is not enough to maintain compulsive drug administration in the drugaddicted subject and that drugs that could interfere with the activation of the striato-thalamo-orbitofrontal circuit could be beneficial in the treatment of drug addiction.

Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex.

An integrated model of drug addiction that encompasses intoxication, bingeing, withdrawal, and craving is proposed, and results imply that addiction connotes cortically regulated cognitive and emotional processes, which result in the overvaluing of drug reinforcers, the undervalued of alternative rein forcers, and deficits in inhibitory control for drug responses.