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      Addiction as Learned Behavior Patterns

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          Abstract

          Individuals with substance use disorders (SUDs) have to cope with drug-related cues and contexts which can affect instrumental drug seeking, as shown with Pavlovian-to-instrumental transfer (PIT) tasks among humans and animals. Our review addresses two potential mechanisms that may contribute to habitual or even compulsive drug seeking and taking. One mechanism is represented by Pavlovian and PIT effects on drug intake. The other is a shift from goal-directed to habitual drug intake, which can be accessed via model-based versus model-free decision-making in respective learning tasks. We discuss the impact of these learning mechanisms on drug consumption. First, we describe how Pavlovian and instrumental learning mechanisms interact in drug addiction. Secondly, we address the effects of acute and chronic stress exposure on behavioral and neural PIT effects in alcohol use disorder (AUD). Thirdly, we discuss how these learning mechanisms and their respective neurobiological correlates can contribute to losing versus regaining control over drug intake. Utilizing mobile technology (mobile applications on smartphones including games that measure learning mechanisms, activity bracelets), computational models, and real-world data may help to better identify patients with a high relapse risk and to offer targeted behavioral and pharmacotherapeutic interventions for vulnerable patients.

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          Most cited references53

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          The neural basis of drug craving: an incentive-sensitization theory of addiction.

          This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.
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            Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On.

            A decade ago, we hypothesized that drug addiction can be viewed as a transition from voluntary, recreational drug use to compulsive drug-seeking habits, neurally underpinned by a transition from prefrontal cortical to striatal control over drug seeking and taking as well as a progression from the ventral to the dorsal striatum. Here, in the light of burgeoning, supportive evidence, we reconsider and elaborate this hypothesis, in particular the refinements in our understanding of ventral and dorsal striatal mechanisms underlying goal-directed and habitual drug seeking, the influence of drug-associated Pavlovian-conditioned stimuli on drug seeking and relapse, and evidence for impairments in top-down prefrontal cortical inhibitory control over this behavior. We further review animal and human studies that have begun to define etiological factors and individual differences in the propensity to become addicted to drugs, leading to the description of addiction endophenotypes, especially for cocaine addiction. We consider the prospect of novel treatments for addiction that promote abstinence from and relapse to drug use.
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              Retraining automatic action tendencies changes alcoholic patients' approach bias for alcohol and improves treatment outcome.

              This study tested the effects of a new cognitive-bias modification (CBM) intervention that targeted an approach bias for alcohol in 214 alcoholic inpatients. Patients were assigned to one of two experimental conditions, in which they were explicitly or implicitly trained to make avoidance movements (pushing a joystick) in response to alcohol pictures, or to one of two control conditions, in which they received no training or sham training. Four brief sessions of experimental CBM preceded regular inpatient treatment. In the experimental conditions only, patients' approach bias changed into an avoidance bias for alcohol. This effect generalized to untrained pictures in the task used in the CBM and to an Implicit Association Test, in which alcohol and soft-drink words were categorized with approach and avoidance words. Patients in the experimental conditions showed better treatment outcomes a year later. These findings indicate that a short intervention can change alcoholics' automatic approach bias for alcohol and may improve treatment outcome.
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                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                24 July 2019
                August 2019
                : 8
                : 8
                : 1086
                Affiliations
                [1 ]Department of Psychiatry and Psychotherapy, Charité–Universitätsmedizin Berlin (Campus Charité Mitte), 10117 Berlin, Germany
                [2 ]Department of Psychiatry and Psychotherapy, Technische Universität Dresden, 01187 Dresden, Germany
                [3 ]Neuroimaging Center, Technische Universität Dresden, 01187 Dresden, Germany
                Author notes
                [* ]Correspondence: siyan908@ 123456hotmail.com
                Author information
                https://orcid.org/0000-0002-6948-5734
                Article
                jcm-08-01086
                10.3390/jcm8081086
                6723628
                31344831
                03e0c5a6-24b6-48ba-94cd-2555561a3218
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 24 June 2019
                : 19 July 2019
                Categories
                Review

                substance use disorders,alternative reward,cue exposure,animal and computational models,behavioral control,craving and relapse,habit formation

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