The dopamine motive system: implications for drug and food addiction

Key Points The motivation to eat, like the motivation to take addictive drugs, activates the forebrain dopamine systems. Excessive activation of this system strengthens the specific habits that precede the activation, sensitizing the animal's responsiveness to the specific conditions that elici...

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Published inNature reviews. Neuroscience Vol. 18; no. 12; pp. 741 - 752
Main Authors Volkow, Nora D., Wise, Roy A., Baler, Ruben
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.12.2017
Nature Publishing Group
Subjects
Online AccessGet full text
ISSN1471-003X
1471-0048
1471-0048
1469-3178
DOI10.1038/nrn.2017.130

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Abstract Key Points The motivation to eat, like the motivation to take addictive drugs, activates the forebrain dopamine systems. Excessive activation of this system strengthens the specific habits that precede the activation, sensitizing the animal's responsiveness to the specific conditions that elicit those habits. At the same time, overactivation of the dopamine system downregulates the dopamine receptors, leaving the subject less interested in other activities. The repeated intake of high-impact foods or addictive drugs thus makes food consumption or drug taking more habitual and decreases the importance of stimuli calling for alternatives. Repeated drug use erodes the function of brain networks necessary for self-regulation, thereby facilitating impulsive, inflexible and compulsive actions. The dopamine motive system, which integrates reinforcement and motivation, is influenced by obesogenic foods and addictive drugs. In this Review, Volkow and colleagues highlight how these stimuli sensitize the subject's motivation towards them while desensitizing the subject's motivation towards alternative reinforcers. Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the reinforcing stimuli (such as drugs or energy-rich foods) that increase the likelihood and/or strength of the behavioural response (such as drug taking or overeating). At a cellular and circuit level, motivational drive is dependent on the concentration of extrasynaptic dopamine present in specific brain areas such as the striatum. Cues that predict a reinforcing stimulus also modulate extrasynaptic dopamine concentrations, energizing motivation. Repeated administration of the reinforcer (drugs, energy-rich foods) generates conditioned associations between the reinforcer and the predicting cues, which is accompanied by downregulated dopaminergic response to other incentives and downregulated capacity for top-down self-regulation, facilitating the emergence of impulsive and compulsive responses to food or drug cues. Thus, dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding. Thus, interventions to rebalance the dopamine motive system might have therapeutic potential for obesity and addiction.
AbstractList Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the reinforcing stimuli (such as drugs or energy-rich foods) that increase the likelihood and/or strength of the behavioural response (such as drug taking or overeating). At a cellular and circuit level, motivational drive is dependent on the concentration of extrasynaptic dopamine present in specific brain areas such as the striatum. Cues that predict a reinforcing stimulus also modulate extrasynaptic dopamine concentrations, energizing motivation. Repeated administration of the reinforcer (drugs, energy-rich foods) generates conditioned associations between the reinforcer and the predicting cues, which is accompanied by downregulated dopaminergic response to other incentives and downregulated capacity for top-down self-regulation, facilitating the emergence of impulsive and compulsive responses to food or drug cues. Thus, dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding. Thus, interventions to rebalance the dopamine motive system might have therapeutic potential for obesity and addiction.
Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the reinforcing stimuli (such as drugs or energy-rich foods) that increase the likelihood and/or strength of the behavioural response (such as drug taking or overeating). At a cellular and circuit level, motivational drive is dependent on the concentration of extrasynaptic dopamine present in specific brain areas such as the striatum. Cues that predict a reinforcing stimulus also modulate extrasynaptic dopamine concentrations, energizing motivation. Repeated administration of the reinforcer (drugs, energy-rich foods) generates conditioned associations between the reinforcer and the predicting cues, which is accompanied by downregulated dopaminergic response to other incentives and downregulated capacity for top-down self-regulation, facilitating the emergence of impulsive and compulsive responses to food or drug cues. Thus, dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding. Thus, interventions to rebalance the dopamine motive system might have therapeutic potential for obesity and addiction.Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the reinforcing stimuli (such as drugs or energy-rich foods) that increase the likelihood and/or strength of the behavioural response (such as drug taking or overeating). At a cellular and circuit level, motivational drive is dependent on the concentration of extrasynaptic dopamine present in specific brain areas such as the striatum. Cues that predict a reinforcing stimulus also modulate extrasynaptic dopamine concentrations, energizing motivation. Repeated administration of the reinforcer (drugs, energy-rich foods) generates conditioned associations between the reinforcer and the predicting cues, which is accompanied by downregulated dopaminergic response to other incentives and downregulated capacity for top-down self-regulation, facilitating the emergence of impulsive and compulsive responses to food or drug cues. Thus, dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding. Thus, interventions to rebalance the dopamine motive system might have therapeutic potential for obesity and addiction.
Key Points The motivation to eat, like the motivation to take addictive drugs, activates the forebrain dopamine systems. Excessive activation of this system strengthens the specific habits that precede the activation, sensitizing the animal's responsiveness to the specific conditions that elicit those habits. At the same time, overactivation of the dopamine system downregulates the dopamine receptors, leaving the subject less interested in other activities. The repeated intake of high-impact foods or addictive drugs thus makes food consumption or drug taking more habitual and decreases the importance of stimuli calling for alternatives. Repeated drug use erodes the function of brain networks necessary for self-regulation, thereby facilitating impulsive, inflexible and compulsive actions. The dopamine motive system, which integrates reinforcement and motivation, is influenced by obesogenic foods and addictive drugs. In this Review, Volkow and colleagues highlight how these stimuli sensitize the subject's motivation towards them while desensitizing the subject's motivation towards alternative reinforcers. Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the reinforcing stimuli (such as drugs or energy-rich foods) that increase the likelihood and/or strength of the behavioural response (such as drug taking or overeating). At a cellular and circuit level, motivational drive is dependent on the concentration of extrasynaptic dopamine present in specific brain areas such as the striatum. Cues that predict a reinforcing stimulus also modulate extrasynaptic dopamine concentrations, energizing motivation. Repeated administration of the reinforcer (drugs, energy-rich foods) generates conditioned associations between the reinforcer and the predicting cues, which is accompanied by downregulated dopaminergic response to other incentives and downregulated capacity for top-down self-regulation, facilitating the emergence of impulsive and compulsive responses to food or drug cues. Thus, dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding. Thus, interventions to rebalance the dopamine motive system might have therapeutic potential for obesity and addiction.
Audience Academic
Author Volkow, Nora D.
Baler, Ruben
Wise, Roy A.
Author_xml – sequence: 1
  givenname: Nora D.
  surname: Volkow
  fullname: Volkow, Nora D.
  email: nvolkow@nida.nih.gov
  organization: National Institute on Drug Abuse, National Institutes of Health
– sequence: 2
  givenname: Roy A.
  surname: Wise
  fullname: Wise, Roy A.
  organization: National Institute on Drug Abuse, National Institutes of Health
– sequence: 3
  givenname: Ruben
  surname: Baler
  fullname: Baler, Ruben
  organization: National Institute on Drug Abuse, National Institutes of Health
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29142296$$D View this record in MEDLINE/PubMed
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Snippet Key Points The motivation to eat, like the motivation to take addictive drugs, activates the forebrain dopamine systems. Excessive activation of this system...
Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational...
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SubjectTerms 59/36
631/378/1488/393
631/378/1689/5
631/378/2629/1788
692/699/317
692/699/476/5
Addiction
Addictions
Analysis
Animal Genetics and Genomics
Animals
Behavior, Addictive - drug therapy
Behavior, Addictive - physiopathology
Behavioral Sciences
Biological Techniques
Biomedicine
Brain research
Dopamine
Dopamine - metabolism
Dopamine - pharmacology
Dopamine receptors
Dopaminergic mechanisms
Drug addiction
Food
Food Addiction - drug therapy
Health aspects
Humans
Motivation
Motivation (Psychology)
Motivation - drug effects
Neostriatum
Neural Pathways - drug effects
Neurobiology
Neurosciences
Obesity
Psychological aspects
Reinforcement (Psychology)
review-article
Risk factors
Title The dopamine motive system: implications for drug and food addiction
URI https://link.springer.com/article/10.1038/nrn.2017.130
https://www.ncbi.nlm.nih.gov/pubmed/29142296
https://www.proquest.com/docview/1978442581
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Volume 18
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