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      Brain serotonin, oxytocin, and their interaction: Relevance for eating disorders

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          Abstract

          Introduction:

          Eating disorders are characterized by maladaptive eating behaviors and preoccupations around body shape, weight, and eating. The serotonin system has been among the most widely studied neurobiological factors in relation to eating disorders. Recent research also highlighted the role of oxytocin.

          Aims and methods:

          This article aims to review animal and human studies on the involvement of central serotonin and oxytocin, and their interplay in eating disorders in particular. We synthesize results from studies using animal models of eating disorders and from research conducted in healthy individuals and clinical populations.

          Results/Outcomes:

          Altered serotonin neurotransmission and oxytocin levels in the brain—particularly in the hypothalamus, brainstem, and limbic regions—were associated with disturbances in eating behaviors and related maladaptive cognitions and emotions. These brain regions were found to constitute a typical neural network through which both central serotonin and oxytocin might operate in a bidirectional manner.

          Conclusions/Interpretation:

          Based on the preceding findings, we describe a developmental biopsychosocial model relevant to eating disorders, including the role of serotonin–oxytocin interactions in the brain. While it is clear that eating disorders are multifactorial in which many biopsychosocial pathways are involved, the current review highlights the importance of well-designed translational research when studying mechanisms of serotonin–oxytocin interactions in the brain. Such research would help to better understand the effects of joint central oxytocin and serotonin administration as a possible preventive or therapeutic intervention for eating disorders.

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          Most cited references200

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          Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals.

          Cells of a multicellular organism are genetically homogeneous but structurally and functionally heterogeneous owing to the differential expression of genes. Many of these differences in gene expression arise during development and are subsequently retained through mitosis. Stable alterations of this kind are said to be 'epigenetic', because they are heritable in the short term but do not involve mutations of the DNA itself. Research over the past few years has focused on two molecular mechanisms that mediate epigenetic phenomena: DNA methylation and histone modifications. Here, we review advances in the understanding of the mechanism and role of DNA methylation in biological processes. Epigenetic effects by means of DNA methylation have an important role in development but can also arise stochastically as animals age. Identification of proteins that mediate these effects has provided insight into this complex process and diseases that occur when it is perturbed. External influences on epigenetic processes are seen in the effects of diet on long-term diseases such as cancer. Thus, epigenetic mechanisms seem to allow an organism to respond to the environment through changes in gene expression. The extent to which environmental effects can provoke epigenetic responses represents an exciting area of future research.
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            Eating disorders

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              • Record: found
              • Abstract: found
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              Is Open Access

              Serotonin and brain function: a tale of two receptors

              Previous attempts to identify a unified theory of brain serotonin function have largely failed to achieve consensus. In this present synthesis, we integrate previous perspectives with new and older data to create a novel bipartite model centred on the view that serotonin neurotransmission enhances two distinct adaptive responses to adversity, mediated in large part by its two most prevalent and researched brain receptors: the 5-HT1A and 5-HT2A receptors. We propose that passive coping (i.e. tolerating a source of stress) is mediated by postsynaptic 5-HT1AR signalling and characterised by stress moderation. Conversely, we argue that active coping (i.e. actively addressing a source of stress) is mediated by 5-HT2AR signalling and characterised by enhanced plasticity (defined as capacity for change). We propose that 5-HT1AR-mediated stress moderation may be the brain’s default response to adversity but that an improved ability to change one’s situation and/or relationship to it via 5-HT2AR-mediated plasticity may also be important – and increasingly so as the level of adversity reaches a critical point. We propose that the 5-HT1AR pathway is enhanced by conventional 5-HT reuptake blocking antidepressants such as the selective serotonin reuptake inhibitors (SSRIs), whereas the 5-HT2AR pathway is enhanced by 5-HT2AR-agonist psychedelics. This bipartite model purports to explain how different drugs (SSRIs and psychedelics) that modulate the serotonergic system in different ways, can achieve complementary adaptive and potentially therapeutic outcomes.
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                Author and article information

                Journal
                J Psychopharmacol
                J Psychopharmacol
                JOP
                spjop
                Journal of Psychopharmacology (Oxford, England)
                SAGE Publications (Sage UK: London, England )
                0269-8811
                1461-7285
                2 January 2025
                March 2025
                : 39
                : 3
                : 187-200
                Affiliations
                [1 ]Eating Disorders Continuum and Research Center, Douglas Mental Health University Institute, Montreal, QC, Canada
                [2 ]Department of Psychology, Concordia University, Montreal, QC, Canada
                [3 ]Department of Molecular Biology, Semmelweis University, Budapest, Hungary
                [4 ]Department of Psychiatry, McGill University, Montreal, QC, Canada
                Author notes
                [*]Linda Booij, Eating Disorders Continuum and Research Center, Douglas Mental Health University Institute, 6605 Boulevard Lasalle, Montreal, QC H4H 1R3, Canada. Email: linda.booij@ 123456mcgill.ca
                Author information
                https://orcid.org/0000-0002-0863-8098
                Article
                10.1177_02698811241309617
                10.1177/02698811241309617
                11843796
                39745000
                9cfe680f-9745-4949-b9e9-bbb6b9a528de
                © The Author(s) 2025

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Funding
                Funded by: Natural Sciences and Engineering Research Council of Canada, FundRef https://doi.org/10.13039/501100000038;
                Award ID: RGPIN/5025-2018
                Funded by: Hungarian National Research Development and Innovation Office, ;
                Award ID: 2019-2.1.11-TÉT-2020-00242
                Categories
                Reviews
                Custom metadata
                ts1

                Pharmacology & Pharmaceutical medicine
                serotonin,oxytocin,brain,eating disorders,social attachment
                Pharmacology & Pharmaceutical medicine
                serotonin, oxytocin, brain, eating disorders, social attachment

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