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      Neural Substrates Underlying Interactions between Appetite Stress and Reward

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          Abstract

          Neurobiological mechanisms that normally control food intake and energy expenditure can be overcome by environmental cues and by stress. Of particular importance is the influence of the mesolimbic reward pathway. In genetically susceptible individuals, problematic over-eating likely reflects a changing balance in the control exerted by homeostatic versus reward circuits that are strongly influenced by environmental factors such as stress. Both stress and activation of the reward pathway have been shown to increase food intake and promote a preference for palatable, high-energy foods. Recent research has focused on the important role of circulating and central neuropeptides that powerfully regulate the brain response to food cues. For example, ghrelin has a potent positive effect on the motivational aspects of food intake, and central oxytocin may be involved in satiety. Thus, the decision to eat, or indeed to over-eat, involves a complex integrated neurobiology that includes brain centres involved in energy balance, reward and stress and their regulation by metabolic and endocrine factors.

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          Most cited references70

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          Oxytocin, vasopressin, and the neurogenetics of sociality.

          There is growing evidence that the neuropeptides oxytocin and vasopressin modulate complex social behavior and social cognition. These ancient neuropeptides display a marked conservation in gene structure and expression, yet diversity in the genetic regulation of their receptors seems to underlie natural variation in social behavior, both between and within species. Human studies are beginning to explore the roles of these neuropeptides in social cognition and behavior and suggest that variation in the genes encoding their receptors may contribute to variation in human social behavior by altering brain function. Understanding the neurobiology and neurogenetics of social cognition and behavior has important implications, both clinically and for society.
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            Addiction-like reward dysfunction and compulsive eating in obese rats: Role for dopamine D2 receptors

            We found that development of obesity was coupled with the emergence of a progressively worsening brain reward deficit. Similar changes in reward homeostasis induced by cocaine or heroin is considered a critical trigger in the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2R) were downregulated in obese rats, similar to previous reports in human drug addicts. Moreover, lentivirus-mediated knockdown of striatal D2R rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuitries and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.
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              'Liking' and 'wanting' food rewards: brain substrates and roles in eating disorders.

              What brain reward systems mediate motivational 'wanting' and hedonic 'liking' for food rewards? And what roles do those systems play in eating disorders? This article surveys recent findings regarding brain mechanisms of hedonic 'liking', such as the existence of cubic-millimeter hedonic hotspots in nucleus accumbens and ventral pallidum for opioid amplification of sensory pleasure. It also considers brain 'wanting' or incentive salience systems important to appetite, such as mesolimbic dopamine systems and opioid motivation circuits that extend beyond the hedonic hotspots. Finally, it considers some potential ways in which 'wanting' and 'liking' might relate to eating disorders.
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                Author and article information

                Journal
                OFA
                OFA
                Obes Facts
                10.1159/issn.1662-4025
                Obesity Facts
                S. Karger AG
                1662-4025
                1662-4033
                2012
                April 2012
                19 April 2012
                : 5
                : 2
                : 208-220
                Affiliations
                aCentre for Integrative Physiology, School of Biomedical Sciences, University of Edinburgh, Edinburgh, UK, bDepartment of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden
                Article
                338237 Obes Facts 2012;5:208–220
                10.1159/000338237
                22647303
                92c75ad2-ec27-4576-b696-ebab49f9568f
                © 2012 S. Karger GmbH, Freiburg

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 15 February 2011
                : 16 June 2011
                Page count
                Pages: 13
                Categories
                Review Article – Food Addiction: Fact or Fiction? – the NeuroFAST Project

                Nutrition & Dietetics,Health & Social care,Public health
                Reward,Stress,Vasopressin,Oxytocin,Ghrelin
                Nutrition & Dietetics, Health & Social care, Public health
                Reward, Stress, Vasopressin, Oxytocin, Ghrelin

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