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      Is Oxytocin “Nature’s Medicine”?

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          Abstract

          Oxytocin is a pleiotropic, peptide hormone with broad implications for general health, adaptation, development, reproduction, and social behavior. Endogenous oxytocin and stimulation of the oxytocin receptor support patterns of growth, resilience, and healing. Oxytocin can function as a stress-coping molecule, an anti-inflammatory, and an antioxidant, with protective effects especially in the face of adversity or trauma. Oxytocin influences the autonomic nervous system and the immune system. These properties of oxytocin may help explain the benefits of positive social experiences and have drawn attention to this molecule as a possible therapeutic in a host of disorders. However, as detailed here, the unique chemical properties of oxytocin, including active disulfide bonds, and its capacity to shift chemical forms and bind to other molecules make this molecule difficult to work with and to measure. The effects of oxytocin also are context-dependent, sexually dimorphic, and altered by experience. In part, this is because many of the actions of oxytocin rely on its capacity to interact with the more ancient peptide molecule, vasopressin, and the vasopressin receptors. In addition, oxytocin receptor(s) are epigenetically tuned by experience, especially in early life. Stimulation of G-protein–coupled receptors triggers subcellular cascades allowing these neuropeptides to have multiple functions. The adaptive properties of oxytocin make this ancient molecule of special importance to human evolution as well as modern medicine and health; these same characteristics also present challenges to the use of oxytocin-like molecules as drugs that are only now being recognized.

          Significance Statement

          Oxytocin is an ancient molecule with a major role in mammalian behavior and health. Although oxytocin has the capacity to act as a “natural medicine” protecting against stress and illness, the unique characteristics of the oxytocin molecule and its receptors and its relationship to a related hormone, vasopressin, have created challenges for its use as a therapeutic drug.

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          Most cited references 293

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          Neuroendocrine perspectives on social attachment and love.

           C Sue Carter (1998)
          The purpose of this paper is to review existing behavioral and neuroendocrine perspectives on social attachment and love. Both love and social attachments function to facilitate reproduction, provide a sense of safety, and reduce anxiety or stress. Because social attachment is an essential component of love, understanding attachment formation is an important step toward identifying the neurobiological substrates of love. Studies of pair bonding in monogamous rodents, such as prairie voles, and maternal attachment in precocial ungulates offer the most accessible animal models for the study of mechanisms underlying selective social attachments and the propensity to develop social bonds. Parental behavior and sexual behavior, even in the absence of selective social behaviors, are associated with the concept of love; the analysis of reproductive behaviors, which is far more extensive than our understanding of social attachment, also suggests neuroendocrine substrates for love. A review of these literatures reveals a recurrent association between high levels of activity in the hypothalamic pituitary adrenal (HPA) axis and the subsequent expression of social behaviors and attachments. Positive social behaviors, including social bonds, may reduce HPA axis activity, while in some cases negative social interactions can have the opposite effect. Central neuropeptides, and especially oxytocin and vasopressin have been implicated both in social bonding and in the central control of the HPA axis. In prairie voles, which show clear evidence of pair bonds, oxytocin is capable of increasing positive social behaviors and both oxytocin and social interactions reduce activity in the HPA axis. Social interactions and attachment involve endocrine systems capable of decreasing HPA reactivity and modulating the autonomic nervous system, perhaps accounting for health benefits that are attributed to loving relationships.
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            Evolution and function of the ADP ribosyl cyclase/CD38 gene family in physiology and pathology.

            The membrane proteins CD38 and CD157 belong to an evolutionarily conserved family of enzymes that play crucial roles in human physiology. Expressed in distinct patterns in most tissues, CD38 (and CD157) cleaves NAD(+) and NADP(+), generating cyclic ADP ribose (cADPR), NAADP, and ADPR. These reaction products are essential for the regulation of intracellular Ca(2+), the most ancient and universal cell signaling system. The entire family of enzymes controls complex processes, including egg fertilization, cell activation and proliferation, muscle contraction, hormone secretion, and immune responses. Over the course of evolution, the molecules have developed the ability to interact laterally and frontally with other surface proteins and have acquired receptor-like features. As detailed in this review, the loss of CD38 function is associated with impaired immune responses, metabolic disturbances, and behavioral modifications in mice. CD38 is a powerful disease marker for human leukemias and myelomas, is directly involved in the pathogenesis and outcome of human immunodeficiency virus infection and chronic lymphocytic leukemia, and controls insulin release and the development of diabetes. Here, the data concerning diseases are examined in view of potential clinical applications in diagnosis, prognosis, and therapy. The concluding remarks try to frame all of the currently available information within a unified working model that takes into account both the enzymatic and receptorial functions of the molecules.
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              Sex differences in anxiety and depression clinical perspectives.

              Sex differences are prominent in mood and anxiety disorders and may provide a window into mechanisms of onset and maintenance of affective disturbances in both men and women. With the plethora of sex differences in brain structure, function, and stress responsivity, as well as differences in exposure to reproductive hormones, social expectations and experiences, the challenge is to understand which sex differences are relevant to affective illness. This review will focus on clinical aspects of sex differences in affective disorders including the emergence of sex differences across developmental stages and the impact of reproductive events. Biological, cultural, and experiential factors that may underlie sex differences in the phenomenology of mood and anxiety disorders are discussed.
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                Author and article information

                Contributors
                Role: ASSOCIATE EDITOR
                Journal
                Pharmacol Rev
                Pharmacol. Rev
                pharmrev
                Pharmacol Rev
                PharmRev
                Pharmacological Reviews
                The American Society for Pharmacology and Experimental Therapeutics (Bethesda, MD )
                0031-6997
                1521-0081
                October 2020
                October 2020
                October 2020
                : 72
                : 4
                : 829-861
                Affiliations
                Kinsey Institute, Indiana University, Bloomington, Indiana (C.S.C., W.M.K., A.M.P., H.P.N., S.W.P.); School of Anthropology, Department of Psychology, and College of Veterinary Medicine, University of Arizona, Tucson, Arizona (E.L.M.); Department of Chemistry, University of Oslo, Oslo, Norway (S.R.W.); Institute of Animal Welfare Science, University of Veterinary Medicine, Vienna, Austria (J.R.Y.); Departments of Psychology and Pharmaceutical Sciences, Northeastern University, Boston, Massachusetts (C.F.F.); Department of Psychiatry, University of Illinois at Chicago, Chicago, Illinois (J.M.D.); Department of Psychology, University of Virginia, Charlottesville, Virginia (J.J.C.); and Department of Pediatrics, Massachusetts General Hospital and Harvard Medical School, Charleston, Massachusetts (M.A.K.)
                Author notes
                Address correspondence to: C. Sue Carter, 428 Lindley Hall, Indiana University, Bloomington, IN 47405. E-mail: suecarterporges@ 123456gmail.com
                Article
                PHARMREV_019398
                10.1124/pr.120.019398
                7495339
                32912963
                Copyright © 2020 by The Author(s)

                This is an open access article distributed under the CC BY-NC Attribution 4.0 International license.

                Page count
                Pages: 33
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