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Reward sensitivity deficits in a rat model of compulsive eating behavior.

Abstract

Compulsive eating behavior is hypothesized to be driven in part by reward deficits likely due to neuroadaptations to the mesolimbic dopamine (DA) system. Therefore, the aim of this study was to assess deficits in reward system functioning and mesolimbic DA after alternating a standard chow with palatable diet, a model of compulsive eating. In this model, rats in the control group (Chow/Chow) are provided a standard chow diet 7 days a week, while the experimental group (Chow/Palatable) is provided chow for 5 days a week ("C Phase"), followed by 2 days of access to a highly palatable sucrose diet ("P Phase"). We first tested the sensitivity to d-Amphetamine's stimulatory, reward-enhancing, and primary rewarding effects using a locomotor activity assay, an intracranial self-stimulation (ICSS) procedure, and a conditioned place preference test, respectively. We then quantified DA release in the nucleus accumbens (NAc) shell after treatment with d-Amphetamine using in vivo microdialysis, quantified levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA using quantitative polymerase chain reaction (qPCR), and lastly, quantified baseline extracellular DA and function of DAT in vivo using quantitative "no-net-flux" microdialysis. Chow/Palatable rats displayed blunted d-Amphetamine-induced locomotor activity, insensitivity to d-Amphetamine potentiation of ICSS threshold, and decreased place preference for d-Amphetamine during the P Phase. We found that Chow/Palatable rats had blunted DA efflux following d-Amphetamine treatment. Furthermore, DAT mRNA was increased in Chow/Palatable rats during the P Phase. Finally, quantitative "no-net-flux" microdialysis revealed reduced extracellular baseline DA and DAT function in Chow/Palatable rats. Altogether, these results provide evidence of reduced reward system functioning and related neuroadaptations in the DA and DAT systems in this model of compulsive eating. Reward deficits, resulting from repeated overeating, may in turn contribute to the perpetuation of compulsive eating behavior.

Authors+Show Affiliations

Laboratory of Addictive Disorders, Departments of Pharmacology and Psychiatry, Boston University School of Medicine, Boston, MA, USA. Graduate Program for Neuroscience, Boston University School of Medicine, Boston, MA, USA.Department of Psychology, Tufts University, Medford, MA, USA.Laboratory of Addictive Disorders, Departments of Pharmacology and Psychiatry, Boston University School of Medicine, Boston, MA, USA.Department of Psychology, Tufts University, Medford, MA, USA. Departments of Neuroscience, Psychiatry and Pharmacology, Tufts University, Boston, MA, USA.Laboratory of Addictive Disorders, Departments of Pharmacology and Psychiatry, Boston University School of Medicine, Boston, MA, USA.Laboratory of Addictive Disorders, Departments of Pharmacology and Psychiatry, Boston University School of Medicine, Boston, MA, USA. cottone@bu.edu.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31622973

Citation

Moore, Catherine F., et al. "Reward Sensitivity Deficits in a Rat Model of Compulsive Eating Behavior." Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 2019.
Moore CF, Leonard MZ, Micovic NM, et al. Reward sensitivity deficits in a rat model of compulsive eating behavior. Neuropsychopharmacology. 2019.
Moore, C. F., Leonard, M. Z., Micovic, N. M., Miczek, K. A., Sabino, V., & Cottone, P. (2019). Reward sensitivity deficits in a rat model of compulsive eating behavior. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, doi:10.1038/s41386-019-0550-1.
Moore CF, et al. Reward Sensitivity Deficits in a Rat Model of Compulsive Eating Behavior. Neuropsychopharmacology. 2019 Oct 17; PubMed PMID: 31622973.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reward sensitivity deficits in a rat model of compulsive eating behavior. AU - Moore,Catherine F, AU - Leonard,Michael Z, AU - Micovic,Nicholas M, AU - Miczek,Klaus A, AU - Sabino,Valentina, AU - Cottone,Pietro, Y1 - 2019/10/17/ PY - 2019/07/29/received PY - 2019/10/08/accepted PY - 2019/10/07/revised PY - 2019/10/18/entrez PY - 2019/10/18/pubmed PY - 2019/10/18/medline JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JO - Neuropsychopharmacology N2 - Compulsive eating behavior is hypothesized to be driven in part by reward deficits likely due to neuroadaptations to the mesolimbic dopamine (DA) system. Therefore, the aim of this study was to assess deficits in reward system functioning and mesolimbic DA after alternating a standard chow with palatable diet, a model of compulsive eating. In this model, rats in the control group (Chow/Chow) are provided a standard chow diet 7 days a week, while the experimental group (Chow/Palatable) is provided chow for 5 days a week ("C Phase"), followed by 2 days of access to a highly palatable sucrose diet ("P Phase"). We first tested the sensitivity to d-Amphetamine's stimulatory, reward-enhancing, and primary rewarding effects using a locomotor activity assay, an intracranial self-stimulation (ICSS) procedure, and a conditioned place preference test, respectively. We then quantified DA release in the nucleus accumbens (NAc) shell after treatment with d-Amphetamine using in vivo microdialysis, quantified levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA using quantitative polymerase chain reaction (qPCR), and lastly, quantified baseline extracellular DA and function of DAT in vivo using quantitative "no-net-flux" microdialysis. Chow/Palatable rats displayed blunted d-Amphetamine-induced locomotor activity, insensitivity to d-Amphetamine potentiation of ICSS threshold, and decreased place preference for d-Amphetamine during the P Phase. We found that Chow/Palatable rats had blunted DA efflux following d-Amphetamine treatment. Furthermore, DAT mRNA was increased in Chow/Palatable rats during the P Phase. Finally, quantitative "no-net-flux" microdialysis revealed reduced extracellular baseline DA and DAT function in Chow/Palatable rats. Altogether, these results provide evidence of reduced reward system functioning and related neuroadaptations in the DA and DAT systems in this model of compulsive eating. Reward deficits, resulting from repeated overeating, may in turn contribute to the perpetuation of compulsive eating behavior. SN - 1740-634X UR - https://www.unboundmedicine.com/medline/citation/31622973/Reward_sensitivity_deficits_in_a_rat_model_of_compulsive_eating_behavior L2 - http://dx.doi.org/10.1038/s41386-019-0550-1 DB - PRIME DP - Unbound Medicine ER -