Oxytocin, vasopressin, and human social behavior Heinrichs, M;von Dawans, B;von Dawans, B; Domes, G (2009 There is substantial evidence from animal research indicating a key role of the neuropeptides oxytocin (OT) and arginine vasopressin (AVP) in the regulation of complex social cognition and behavior. As social interaction permeates the whole of human society, and the fundamental ability to form attachment is indispensable for social relationships, studies are beginning to dissect the roles of OT and AVP in human social behavior. New experimental paradigms and technologies in human research allow a more nuanced investigation of the molecular basis of social behavior. In addition, a better understanding of the neurobiology and neurogenetics of human social cognition and behavior has important implications for the current development of novel clinical approaches for mental disorders that are associated with social deficits (e.g., autism spectrum disorder, social anxiety disorder, and borderline personality disorder). This review focuses on our recent knowledge of the behavioral, endocrine, genetic, and neural effects of OT and AVP in humans and provides a synthesis of recent advances made in the effort to implicate the oxytocinergic system in the treatment of psychopathological states. t r a c tThere is substantial evidence from animal research indicating a key role of the neuropeptides oxytocin (OT) and arginine vasopressin (AVP) in the regulation of complex social cognition and behavior. As social interaction permeates the whole of human society, and the fundamental ability to form attachment is indispensable for social relationships, studies are beginning to dissect the roles of OT and AVP in human social behavior. New experimental paradigms and technologies in human research allow a more nuanced investigation of the molecular basis of social behavior. In addition, a better understanding of the neurobiology and neurogenetics of human social cognition and behavior has important implications for the current development of novel clinical approaches for mental disorders that are associated with social deficits (e.g., autism spectrum disorder, social anxiety disorder, and borderline personality disorder). This review focuses on our recent knowledge of the behavioral, endocrine, genetic, and neural effects of OT and AVP in humans and provides a synthesis of recent advances made in the effort to implicate the oxytocinergic system in the treatment of psychopathological states.

No abstract

No abstract

The neuropeptide oxytocin has played an essential role in the regulation of social behavior and attachment throughout mammalian evolution. Because recent studies in humans have shown that oxytocin administration reduces stress responses and increases prosocial behavior, we investigated whether a common single nucleotide polymorphism (rs53576) in the oxytocin receptor gene (OXTR) might interact with stress-protective effects of social support. Salivary cortisol samples and subjective stress ratings were obtained from 194 healthy male participants before, during, and after a standardized psychosocial laboratory stress procedure. Participants were randomly assigned either to prepare alone or to receive social support from their female partner or close female friend while preparing for the stressful task. Differential stress responses between the genotype groups were observed depending on the presence or absence of social support. Only individuals with one or two copies of the G allele of rs53576 showed lower cortisol responses to stress after social support, compared with individuals with the same genotype receiving no social support. These results indicate that genetic variation of the oxytocin system modulates the effectiveness of positive social interaction as a protective buffer against a stressful experience.

Psychosocial stress precipitates a wide spectrum of diseases with major public-health significance. The fight-or-flight response is generally regarded as the prototypic human stress response, both physiologically and behaviorally. Given that having positive social interactions before being exposed to acute stress plays a preeminent role in helping individuals control their stress response, engaging in prosocial behavior in response to stress (tend-and-befriend) might also be a protective pattern. Little is known, however, about the immediate social responses following stress in humans. Here we show that participants who experienced acute social stress, induced by a standardized laboratory stressor, engaged in substantially more prosocial behavior (trust, trustworthiness, and sharing) compared with participants in a control condition, who did not experience socioevaluative threat. These effects were highly specific: Stress did not affect the readiness to exhibit antisocial behavior or to bear nonsocial risks. These results show that stress triggers social approach behavior, which operates as a potent stress-buffering strategy in humans, thereby providing evidence for the tend-and-befriend hypothesis.

No abstract

No abstract

The present study experimentally tested the cross-stressor adaptation hypothesis by examining whether endurance exercise training leads to reductions in the physiological stress response to a psychosocial stressor. We randomly assigned 149 healthy men to a 12-week exercise training, relaxation training, or a wait list control group. Before and after intervention we assessed the groups' physical fitness (lactate testing) and compared their physiological stress responses to the Trier Social Stress Test for Groups in terms of salivary free cortisol, heart rate (HR) and heart rate variability (HRV); the final sample consisted of 96 subjects. As hypothesized, the exercise training significantly improved fitness and reduced stress reactivity in all three parameters; however, it only improved stress recovery in terms of HR. The relaxation program reduced only cortisol, but not HR or HRV reactivity; no changes emerged for the control group. The findings suggest that the cross-stressor adaptation hypothesis is valid for cardiovascular as well as endocrine stress reactivity.