Oxytocin, a neuropeptide known for its role in reproduction and socioemotional processes, may hold promise as a therapeutic agent in treating social impairments in patient populations. However, research has yet to uncover precisely how to manipulate this system for clinical benefit. Moreover, inconsistent use of standardized and validated oxytocin measurement methodologies-including the design and study of hormone secretion and biochemical assays-present unresolved challenges. Human studies measuring peripheral (i.e., in plasma, saliva, or urine) or central (i.e., in cerebrospinal fluid) oxytocin concentrations have involved very diverse methods, including the use of different assay techniques, further compounding this problem. In the present review, we describe the scientific value in measuring human endogenous oxytocin concentrations, common issues in biochemical analysis and study design that researchers face when doing so, and our recommendations for improving studies using valid and reliable methodologies.
Abstract Chronic stress is known to enhance the susceptibility for addiction disorders including alcoholism. While these findings have been recapitulated in animal models, the majority of these studies have utilized non‐social rather than social stress paradigms; the latter of which are believed to be more relevant to the human situation. Therefore, the major aim of this study was to investigate, if 14 days of chronic subordinate colony housing ( CSC ), a pre‐clinically validated psychosocial stress paradigm relevant for human psychiatric and somatic disorders, enhances ethanol ( EtOH ) consumption in male mice. To assess this, we employed the well‐established two‐bottle free‐choice paradigm where mice were given access to water and 2, 4, 6 and 8% EtOH solutions (with the concentrations increasing each fourth day) following termination of the stress procedure. After 14 days of CSC , stressed mice consumed significantly more EtOH at all concentrations tested and displayed increased EtOH preference at concentrations of 6 and 8%. This effect was not due to an altered taste preference in CSC mice as assessed by saccharine‐ and quinine‐preference tests, but was accompanied by increased anxiety‐related behavior. Systemic administration of baclofen (2.5 mg/kg) or oxytocin ( OXT ; 10 mg/kg) reduced the EtOH intake in single housed control (baclofen, OXT ) and CSC (baclofen) mice, whereas intracerebroventricular OXT (0.5 μ g/2 μl ) was ineffective in both groups. Taken together, these results suggest that (i) chronic psychosocial stress enhances EtOH consumption, and (ii) baclofen and OXT differentially affect EtOH intake in mice.
Aggression causes major health and social problems and constitutes a central problem in several psychiatric disorders. There is a close relationship between the display of aggression and stress coping strategies. In order to gain more insight into biochemical pathways associated with aggression and stress coping, we assessed behavioral and neurobiological responses in two genetically selected rodent models, namely wild house mice selectively bred for a short (SAL) and long (LAL) attack latency and Wistar rats bred for high (HAB) or low (LAB) anxiety-related behavior. Compared to their line counterparts, the SAL mice and the LAB rats display a high level of intermale aggression associated with a proactive coping style. Both the SAL mice and the LAB rats show a reduced hypothalamic-pituitary-adrenal (HPA) axis response to non-social stressors. However, when exposed to social stressors (resident-intruder, sensory contact), SAL mice show an attenuated HPA response, whereas LAB rats show an elevated HPA response. In both rodent lines, the display of aggression is associated with high neuronal activation in the central amygdala, but reduced neuronal activation in the lateral septum. Furthermore, in the lateral septum, SAL mice have a reduced vasopressinergic fiber network, and LAB rats show a decreased vasopressin release during the display of aggression. Moreover, the two lines show several indications of an increased serotonergic neurotransmission. The relevance of these findings in relation to high aggression and stress coping is discussed. In conclusion, exploring neurobiological systems in animals sharing relevant behavioral characteristics might be a useful approach to identify general mechanisms of action, which in turn can improve our understanding of specific behavioral symptoms in human psychiatric disorders.
The peripartum period is a time of high susceptibility for mood and anxiety disorders, some of which have recently been associated with alterations in hippocampal neurogenesis. Several factors including stress, aging, and, perhaps unexpectedly, lactation have been shown to decrease hippocampal neurogenesis. Intriguingly, lactation is also a time of reduced stress responsivity suggesting that the effect of stress on neurogenic processes may differ during this period. Therefore, the aim of the present study was to assess the effect of repeated stress during lactation [2 h restraint stress from lactation day (LD) 2 to LD13] on brain weight, hippocampal volume, cell proliferation and survival, and on neuronal and astroglial differentiation. In addition to confirming the known lactation-associated decrease in cell proliferation and survival, we could reveal that stress reversed the lactation-induced decrease in cell proliferation, while it did not affect survival of newly born cells, nor the number of mature neurons , nor did it alter immature neuron production or the number of astroglial cells in lactation. Stress exposure increased relative brain weight and hippocampal volume mirroring the observed changes in neurogenesis. Interestingly, hippocampal volume and relative brain weight were lower in lactation as compared to nulliparous females under nonstressed conditions. This study assessed the effect of stress during lactation on hippocampal neurogenesis and indicates that stress interferes with important peripartum adaptations at the level of the hippocampus.
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