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"Oxytocin is a neurohypophysial hormone that consists of nine amino acids which are synthesized in the paraventricular, supraoptic, and accessory nuclei of the hypothalamus. Oxytocin is released in systemic blood circulation through the posterior pituitary gland, where it acts as hormone, regulating a range of physiological functions. It is involved in learning and memory, sensory and motor regulation via the spinal cord and regulation of the reproductive system. The quality and stability of one's romantic relationship can impact overall well-being and health, leading researchers to search for the mechanisms that underlie the development of relationship discord versus those that foster satisfaction. Within this field, there has been recent attention towards biological variables, with oxytocin being at the forefront due to its established role in pair bonding in both animals and humans. A review is presented which suggests the involvement of the oxitocinergic system in the regulation of the hypothalamic-pituitary-gonadal-axis during pubertal development and social cognition in mammals. The closing study presents data which indicate that oxytocin has actions in different brain areas and is involved with spine-specific plastic effects, and modulates the dynamic neural sex steroid actions and the processing of context-dependent stimuli by adapting the neuronal and synaptic structure to the reproductive status and the social experience in mice"--

Oxytocin.

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

oxytocin --- AVPR1A gene --- gender --- age --- trust game

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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.

Cerebellum --- Striatum --- Oxytocin --- mTOR --- Hypothalamus --- Neurodevelopmental disorders --- Cell signaling

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Oxytocin (OT) and arginine vasopressin (AVP) are the paramount social hormones in mammals and accumulating evidence also strengthens the unique role of these neuropeptides also in human social behavior. Indeed from voles to humans, OT and AVP modulate an intriguing number of social behaviors resonating across species such as the quality of pair bonding, parenting, modulations of social stress, in-group & out-group relationships and social communications. Recent molecular genetic studies of the oxytocin (OXTR), arginine vasopressin 1a (AVPR1a) and arginine vasopressin 1b (AVPR1b) receptors have strengthened the role of these two neuropeptides in a range of normal and pathological human behaviors. Importantly, dysfunctions in the OT and AVP neural pathways are likely contributing to deficits in social skills and communication in disorders such as autism. This Research Topic covers the state of the science and provides a deep view of social hormone research in humans to illustrates how pharmacological, genetic and neuroimaging strategies can be successfully combined toward unraveling the mystery of how human social behavior is regulated. Understanding human social behavior at the molecular level, i.e. social neuroscience, is not only crucial for treatment and diagnosis of disorders characterized by deficits in social cognition but also has important implications in establishing the congruence of findings from different approaches in the Social Sciences and Biology. We bring together in this issue a broad spectrum of investigators from the neurosciences, genetics, psychology, economics and political science towards a deeper understanding of the biological roots of human social behavior. We hope that this transdisciplinary Research Topic will bring new insights and ideas to the field, give future perspectives while also addressing open questions and limitation in order to develop intervention and prevention strategies, and to translate the basic social hormone research into clinical applications. This Research Topic covers the state of the science and provides a deep view of social hormone research in humans to illustrates how pharmacological, genetic and neuroimaging strategies can be successfully combined toward unraveling the mystery of how human social behavior is regulated. Understanding human social behavior at the molecular level, aka social neuroscience, is not only crucial for treatment and diagnosis of disorders characterized by deficits in social cognition but such an understanding has important implications for consilience of the Social Sciences and Biology. We bring together in this issue a broad spectrum of investigators from the neurosciences, genetics, psychology, economics and political science towards a deeper understanding of the biological roots of human social behavior. We hope that this transdisciplinary Research Topic will bring new insights and ideas to the field, give future perspectives while also addressing open questions and limitation in order to develop intervention and prevention strategies, and to translate the basic social hormone research into clinical applications.

Human behavior. --- Hormones. --- receptor --- Oxytocin --- receptors --- Social Behavior --- CD38 --- intranasal --- Psychiatry

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Anti-social behaviors and social deficits induced mental disorders are critical problems in our society today. Social behaviors and interactions are shaped by experience, hereditary components (genes, hormones and neuropeptides) and environmental factors (photoperiods and metabolic signals). In addition to the classical gonadotropin-releasing hormone, RFamide peptides, kisspeptin and gonadotropin-inhibiting hormone are emerging as important regulators of the reproductive axis. These neuropeptides are evolutionarily conserved and are regulated by environmental factors. In this Research Topic, we advocate more recent advances in reproductive neuropeptides and sex steroids in the domains of social behavior including sexual and parental behavior, aggression, stress and anxiety. Using multiple species model, we also review how genes and the neuroendocrine system interact at the cell and organismic levels to contribute to social behavior in particular the epigenetic genomic changes caused by early life environment. We provide comprehensive insights of distinct neural networks and how cellular and molecular events in the brain regulate social behavior from a comparative perspective.

sex steroids --- HPG axis --- Reproduction --- Oxytocin --- Aggression --- vasopressin --- Behavior --- GnRH --- neurotransmitter --- social bonding