ArticleObesity (Silver Spring, Md.)2016
Binge-type eating disrupts dopaminergic and GABAergic signaling in the prefrontal cortex and ventral tegmental area.
Article in Obesity (Silver Spring, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Systematic Review of Binge Eating Rodent Models for Developing Novel or Repurposing Existing Pharmacotherapies.Biomolecules · 2023Pooled it
- Binge Eating and Obesity Differentially Alter the Mesolimbic Endocannabinoid System in Rats.International journal of molecular sciences · 2025Article
- The emerging role of glucagon-like peptide 1 in binge eating.The Journal of endocrinology · 2024Review
- The Role of the Endocannabinoid System in Binge Eating Disorder.International journal of molecular sciences · 2023Review
- Corticostriatal dynamics underlying components of binge-like consumption of palatable food in mice.Appetite · 2023Article
- A literature review of dopamine in binge eating.Journal of eating disorders · 2022Review
- Pairing Binge Drinking and a High-Fat Diet in Adolescence Modulates the Inflammatory Effects of Subsequent Alcohol Consumption in Mice.International journal of molecular sciences · 2021Article
- Bingeing on High-Fat Food Enhances Evoked Dopamine Release and Reduces Dopamine Uptake in the Nucleus Accumbens.Obesity (Silver Spring, Md.) · 2021Article
- Binge-like palatable food intake in rats reduces preproglucagon in the nucleus tractus solitarius.Physiology & behavior · 2020Article
- VIPergic neurons of the infralimbic and prelimbic cortices control palatable food intake through separate cognitive pathways.JCI insight · 2019Article
- Binge-Type Eating in Rats is Facilitated by Neuromedin U Receptor 2 in the Nucleus Accumbens and Ventral Tegmental Area.Nutrients · 2019Article
- Reduced Medial Prefrontal Control of Palatable Food Consumption Is Associated With Binge Eating Proneness in Female Rats.Frontiers in behavioral neuroscience · 2019Article
- Dopamine in the oval bed nucleus of the stria terminalis contributes to compulsive responding for sucrose in rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Noradrenaline transporter availability on [European journal of nuclear medicine and molecular imaging · 2018Article
- Limited Access to a High Fat Diet Alters Endocannabinoid Tone in Female Rats.Frontiers in neuroscience · 2018Article
- Cognitive impairment and gene expression alterations in a rodent model of binge eating disorder.Physiology & behavior · 2017Article
- A Potential Animal Model of Maladaptive Palatable Food Consumption Followed by Delayed Discomfort.Frontiers in neuroscience · 2017Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectiveBinge eating is characterized by repeated intermittent bouts of compulsive overconsumption of food. Treatment is challenging given limited understanding of the mechanisms underlying this type of disordered eating. The hypothesis that dysregulation of mesocortical dopaminergic and GABAergic systems underlie binge eating was tested.
methodsAnalysis of gene expression within the ventral tegmental area and its terminal mesocortical regions was examined in bingeing rats before and after bingeing occurred. In addition, alterations in binge-type behavior induced by pharmacological inactivation of subnuclei of the prefrontal cortex (PFC) and by pharmacological activation and inhibition of cortical D1 and D2 receptors were examined.
resultsCorrelative and functional evidence demonstrates dysregulated neurotransmitter processing by the PFC and ventral tegmental area, but not the amygdala or nucleus accumbens, in bingeing rats. Either GABAergic inactivation or D2-like receptor activation within the PFC increased consumption in bingeing rats, but not controls, suggesting that the PFC, and D2 receptors in particular, functions as a behavioral brake to limit bingeing.
conclusionsThe act of bingeing resolved some gene expression differences that preceded binge onset, further suggesting that bingeing may partially serve to self-medicate a system driving this maladaptive behavior. However, the failure of bingeing to resolve other dopaminergic/GABAergic differences may render individuals vulnerable to future binge episodes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.