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      The incentive sensitization theory of addiction: some current issues

      1 , 1

      Philosophical Transactions of the Royal Society B: Biological Sciences

      The Royal Society

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          Abstract

          We present a brief overview of the incentive sensitization theory of addiction. This posits that addiction is caused primarily by drug-induced sensitization in the brain mesocorticolimbic systems that attribute incentive salience to reward-associated stimuli. If rendered hypersensitive, these systems cause pathological incentive motivation ('wanting') for drugs. We address some current questions including: what is the role of learning in incentive sensitization and addiction? Does incentive sensitization occur in human addicts? Is the development of addiction-like behaviour in animals associated with sensitization? What is the best way to model addiction symptoms using animal models? And, finally, what are the roles of affective pleasure or withdrawal in addiction?

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          Most cited references 77

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          A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes.

          Contemporary urge models assume that urges are necessary but not sufficient for the production of drug use in ongoing addicts, are responsible for the initiation of relapse in abstinent addicts, and can be indexed across 3 classes of behavior: verbal report, overt behavior, and somatovisceral response. A review of available data does not provide strong support for these assumptions. An alternative cognitive model of drug use and drug urges is proposed that hypothesizes that drug use in the addict is controlled by automatized action schemata. Urges are conceptualized as responses supported by nonautomatic cognitive processes activated in parallel with drug-use action schemata either in support of the schema or in support of attempts to block the execution of the schema. The implications of this model for the assessment of urge responding and drug-use behavior are presented.
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            Addiction.

            The development of addiction involves a transition from casual to compulsive patterns of drug use. This transition to addiction is accompanied by many drug-induced changes in the brain and associated changes in psychological functions. In this article we present a critical analysis of the major theoretical explanations of how drug-induced alterations in psychological function might cause a transition to addiction. These include: (a) the traditional hedonic view that drug pleasure and subsequent unpleasant withdrawal symptoms are the chief causes of addiction; (b) the view that addiction is due to aberrant learning, especially the development of strong stimulus-response habits; (c) our incentive-sensitization view, which suggests that sensitization of a neural system that attributes incentive salience causes compulsive motivation or "wanting" to take addictive drugs; and (d) the idea that dysfunction of frontal cortical systems, which normally regulate decision making and inhibitory control over behavior, leads to impaired judgment and impulsivity in addicts.
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              Transition from moderate to excessive drug intake: change in hedonic set point.

               P Ahmed,  K Koob (1998)
              Differential access to cocaine self-administration produced two patterns of drug intake in rats. With 1 hour of access per session, drug intake remained low and stable. In contrast, with 6 hours of access, drug intake gradually escalated over days. After escalation, drug consumption was characterized by an increased early drug loading and an upward shift in the cocaine dose-response function, suggesting an increase in hedonic set point. After 1 month of abstinence, escalation of cocaine intake was reinstated to a higher level than before. These findings may provide an animal model for studying the development of excessive drug intake and the basis of addiction.
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                Author and article information

                Journal
                Philosophical Transactions of the Royal Society B: Biological Sciences
                Phil. Trans. R. Soc. B
                The Royal Society
                0962-8436
                1471-2970
                July 24 2008
                October 12 2008
                July 18 2008
                October 12 2008
                : 363
                : 1507
                : 3137-3146
                Affiliations
                [1 ]Department of Psychology (Biopsychology Program), The University of MichiganEast Hall, 530 Church Street, Ann Arbor, MI 48109, USA
                Article
                10.1098/rstb.2008.0093
                2607325
                18640920
                © 2008

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