Addiction: a disease of learning and memory.
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 that addiction represents a pathological usurpation of the neural mechanisms of learning and memory that under normal circumstances serve to shape survival behaviors related to the pursuit of rewards and the cues that predict them. The author summarizes the converging evidence in this area and highlights key questions that remain.
Hyman
Steven E
SE
Department of Neurobiology, Harvard Medical School, Boston, MA, USA. seh@harvard.edu
D000818:Animals; D016739:Behavior, Addictive / Q000503:physiopathology / Q000523:psychology; D003463:Cues; D004298:Dopamine / Q000502:physiology*; D004399:Dynorphins / Q000502:physiology; D005971:Glutamates / Q000502:physiology; D006801:Humans; D007858:Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D008959:Models, Neurological; D008960:Models, Psychological; D009473:Neuronal Plasticity / Q000502:physiology; D017397:Prefrontal Cortex / Q000502:physiology; D051381:Rats; D012008:Recurrence; D012201:Reward; D019966:Substance-Related Disorders / Q000503:physiopathology* / Q000523:psychology
D005971:Glutamates; D004399:Dynorphins; D004298:Dopamine