Recovering drug addicts encounter danger when faced with drug-related cues or contexts, because those situations can trigger relapse. Similarly, bouts of binge eating are often triggered by cues for food relevant rewards. Cues are especially potent triggers when individuals are in vulnerable states. These proposal aims to identify the brain states that cause vulnerability to cue-triggered 'wanting'of reward. The responsible brain mechanisms particularly involve the limbic nucleus accumbens and amygdala. Here we will study how these brain mechanisms cause excessive incentive salience ('wanting') to be attributed to particular reward cues. In experiment 1, microinjections of agonist drugs and a Fos plume mapping tool will be used to identify the neural mechanisms in nucleus accumbens and amygdala that magnify cue-triggered 'wanting'. In experiment 2, the circuit principles that join together the nucleus accumbens and amygdala into a cooperative system will be identified by manipulating the structures with multiple simultaneous microinjections. In experiment 3, prior neural sensitization and learning manipulations will help show how natural 'wanting'mechanisms are usurped by drugs and sensitization to cause an addicted reward to be 'wanted'more than other rewards. These studies will help clarify the brain and psychological mechanisms that cause addicts to excessively 'want'drug and binge eaters to excessively 'want'food rewards.

Public Health Relevance

A primary problem in drug addiction and binge eating disorders is the continuing danger for relapse posed by encounters with cues for the addicted reward (even after long periods of abstinence). A brain mechanism has been hypothesized to cause cue-triggered relapse, namely incentive sensitization of brain systems that generate normal 'wanting' for rewards. The studies proposed here will help reveal those brain mechanisms underlying cue-triggered relapse, and will shed light on how compulsive 'wants'are produced in addiction and in eating disorders.

National Institute of Health (NIH)
National Institute on Drug Abuse (NIDA)
Research Project (R01)
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Biobehavioral Regulation, Learning and Ethology Study Section (BRLE)
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Volman, Susan
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University of Michigan Ann Arbor
Schools of Arts and Sciences
Ann Arbor
United States
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Berridge, Kent C (2018) Evolving Concepts of Emotion and Motivation. Front Psychol 9:1647
Cole, Shannon L; Robinson, Mike J F; Berridge, Kent C (2018) Optogenetic self-stimulation in the nucleus accumbens: D1 reward versus D2 ambivalence. PLoS One 13:e0207694
Olney, Jeffrey J; Warlow, Shelley M; Naffziger, Erin E et al. (2018) Current perspectives on incentive salience and applications to clinical disorders. Curr Opin Behav Sci 22:59-69
Badiani, Aldo; Berridge, Kent C; Heilig, Markus et al. (2018) Addiction research and theory: a commentary on the Surgeon General's Report on alcohol, drugs, and health. Addict Biol 23:3-5
Mitchell, Marci R; Berridge, Kent C; Mahler, Stephen V (2018) Endocannabinoid-Enhanced ""Liking"" in Nucleus Accumbens Shell Hedonic Hotspot Requires Endogenous Opioid Signals. Cannabis Cannabinoid Res 3:166-170
Castro, Daniel C; Berridge, Kent C (2017) Opioid and orexin hedonic hotspots in rat orbitofrontal cortex and insula. Proc Natl Acad Sci U S A 114:E9125-E9134
Warlow, Shelley M; Robinson, Mike J F; Berridge, Kent C (2017) Optogenetic Central Amygdala Stimulation Intensifies and Narrows Motivation for Cocaine. J Neurosci 37:8330-8348
Kringelbach, Morten L; Berridge, Kent C (2017) The Affective Core of Emotion: Linking Pleasure, Subjective Well-Being, and Optimal Metastability in the Brain. Emot Rev 9:191-199
Berridge, Kent C (2017) Is Addiction a Brain Disease? Neuroethics 10:29-33
Song, Cai; Berridge, Kent C; Kalueff, Allan V (2016) 'Stressing' rodent self-grooming for neuroscience research. Nat Rev Neurosci 17:591

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