Psychoneuroendocrinology RSS feed: Current Issue. Psychoneuroendocrinology publishes papers dealing with the interrelated disciplines of psychology, neurobiology, endocrinology, immunology, neurology, and psychiatry, with an emphasis on multidisciplinary studies aiming at integrating these disciplines in terms of either basic research or clinical implications. One of the main goals is to understand how a variety of psychobiological factors interact in the expression of the stress response as it relates to the development and/or maintenance of neuropsychiatric illnesses. The journal is international and comprises original research papers, reviews of an area of the literature, or at an appropriate stage in the development of the author's own work, commentaries in areas of current interest, short communications and book reviews. Although reviews, editorials and commentaries are usually by invitation, interested authors can contact one of the Co-Editors-in-Chief to discuss the suitability of topics for either category of manuscripts. Electronic usage An increasing number of readers access the journal online via ScienceDirect, one of the world's most advanced web delivery systems for scientific, technical and medical information. http://www.psyneuen-journal.com/?rss=yesElsevier Inc.en © 2012 Published by Elsevier Inc. All rights reserved. Psychoneuroendocrinology0306-4530373March 2012 © 2012 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.psyneuen-journal.com/article/PIIS0306453012000042/abstract?rss=yesEditorial Board10.1016/S0306-4530(12)00004-2Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7CO2CO2http://www.psyneuen-journal.com/article/PIIS0306453011003702/abstract?rss=yesSummary: Exposure to psychosocial stress has been associated with increasing rates of morbidity in humans and in animal models, but the underlying mechanisms are not completely understood. Major stress responsive systems, such as the hypothalamus-pituitary adrenal (HPA) axis and the autonomic nervous system (ANS) are under investigation as underlying pathways, but although acute stress reliably activates these systems, findings of long-term alternations in baseline activity are inconsistent at present. Emerging evidence suggests that stress-related changes in the sensitivity of target systems toward glucocorticoid (GC) regulation, i.e. development of GC resistance, might help explain inflammatory disinhibition and development of disease related to inflammation. More recent findings further show that the autonomic nervous system might play an important role in the regulatory control of the inflammatory cascade. The major argument put forward in this manuscript is that target tissues for stress system modulation, such as the inflammatory cascade, vary in their ability to respond to stress system signaling, and that assessing alterations in this stress signal sensitivity which can be caused by stress or disease processes, might be necessary to understand and explain stress effects on health. This review focuses on the inflammatory system in particular, because anti-inflammatory effects of most stress systems have been documented, but the general assumption might have to be generalized to other target systems. The main conclusion to be made is that reduction in glucocorticoid sensitivity of target tissues is the most consistent finding at present, and that assessing such changes in glucocorticoid sensitivity might be necessary to understand many stress-related changes in physiology.Acute and chronic stress induced changes in sensitivity of peripheral inflammatory pathways to the signals of multiple stress systems – 2011 Curt Richter Award WinnerNicolas Rohleder10.1016/j.psyneuen.2011.12.015Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-72011 Curt P. Richter Award Winner307316http://www.psyneuen-journal.com/article/PIIS0306453011001880/abstract?rss=yesSummary: Background: Hypothalamic–pituitary–adrenal (HPA)-axis dysregulation has inconsistently been associated with posttraumatic stress disorder (PTSD). Yet, trauma exposure rather than PTSD may be responsible for HPA-axis dysregulation. In two meta-analyses, we assessed the association of adulthood trauma exposure and HPA-axis functioning in healthy subjects with and without PTSD.Method: A literature search in Pubmed and PsychInfo, using keywords and MeSH terms such as cortisol, emotional trauma, and PTSD, was performed. Only studies that included mentally healthy trauma-exposed (TE) individuals as well as non-exposed (NE) healthy individuals and/or PTSD patients (PTSD) were selected. This resulted in 1511 studies of which ultimately, 37 studies (21 TE versus NE and 34 TE versus PTSD, N=2468) were included. Methodological quality of all studies was assessed according to specific quality criteria. Pooled effect sizes (Hedges's g) on cortisol levels were compared. For all analyses, random effect models were used.Results: Cortisol levels were neither significantly different between TE versus NE subjects (−0.029; 95%CI: −0.145; 0.088) nor between TE subjects versus PTSD patients (0.175; 95%CI: −0.012; −0.362). Subgroup analyses showed an increased cortisol suppression after the low dose dexamethasone suppression test (DST) in TE versus NE subjects (−0.509; 95%CI: −0.871; −0.148). This meta-analysis was limited by the fact that lifetime psychiatric illness and childhood trauma were not an exclusion criterion in all 37 studies.Conclusion: Neither adulthood trauma exposure nor PTSD were associated with differences in HPA-axis functioning, although adulthood trauma may augment cortisol suppression after the DST. More evidence on other dynamic tests of HPA-axis functioning in PTSD and adulthood trauma exposure is needed.Adulthood trauma and HPA-axis functioning in healthy subjects and PTSD patients: A meta-analysisEllen R. Klaassens, Erik J. Giltay, Pim Cuijpers, Tineke van Veen, Frans G. Zitman10.1016/j.psyneuen.2011.07.003Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Review317331http://www.psyneuen-journal.com/article/PIIS0306453011001855/abstract?rss=yesSummary: Background: Functional somatic symptoms (FSS), like chronic pain and overtiredness, are often assumed to be stress-related. Altered levels of the stress hormone cortisol could explain the association between stress and somatic complaints. We hypothesized that low cortisol levels after awakening and low cortisol levels during stress are differentially associated with specific FSS.Methods: This study is performed in a subsample of TRAILS (Tracking Adolescents’ Individual Lives Survey) consisting of 715 adolescents (mean age: 16.1years, SD=0.6, 51.3% girls). Adolescents’ cortisol levels after awakening and during a social stress task were assessed. The area under the curve with respect to the ground (AUCg) and the area under the curve above the baseline (AUCab) were calculated for these cortisol levels. FSS were measured using the Youth Self-Report and pain questions. Based upon a factor analysis, FSS were divided into two clusters, one consisting of headache and gastrointestinal symptoms and the other consisting of overtiredness, dizziness and musculoskeletal pain.Results: Regression analyses revealed that the cluster of headache and gastrointestinal symptoms was associated with a low AUCg of cortisol levels during stress (β=−.09, p=.03) and the cluster of overtiredness, dizziness and musculoskeletal pain with a low AUCg of cortisol levels after awakening (β=−.15, p=.008). All these analyses were adjusted for the potential confounders smoking, physical activity level, depression, corticosteroid use, oral contraceptive use, gender, body mass index and, if applicable, awakening time.Conclusion: Two clusters of FSS are differentially associated with the stress hormone cortisol.Symptom-specific associations between low cortisol responses and functional somatic symptoms: The TRAILS studyKarin A.M. Janssens, Albertine J. Oldehinkel, Frank C. Verhulst, Joke A.M. Hunfeld, Johan Ormel, Judith G.M. Rosmalen10.1016/j.psyneuen.2011.06.016Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles332340http://www.psyneuen-journal.com/article/PIIS0306453011001867/abstract?rss=yesSummary: The present study examined the relationship between ageing, physical function and the diurnal rhythms of cortisol and dehydroepiandrosterone (DHEA). Participants were 36 community dwelling older adults aged between 65 and 86 years old. Salivary cortisol and DHEA were measured over the course of one day: immediately upon awakening, 30min later, and then 3h, 6h, 9h and 12h post-awakening. Participants completed the Nottingham extended activities of daily living index, the Berg Balance Scale and their handgrip strength was assessed. Older participants had a significantly higher cortisol area under the curve (AUC), lower overall DHEA levels, lower DHEA AUC, a decreased diurnal slope of decline and increased cortisol:DHEA ratio. Lower diurnal cortisol levels were associated with poorer performance on the Berg Balance Scale and lower handgrip strength, and those with a flattened DHEA diurnal profile reported less independence in carrying out daily tasks. These associations withstood adjustment for age. In conclusion, this study suggests an association between cortisol, DHEA, ageing and physical function.Ageing, physical function, and the diurnal rhythms of cortisol and dehydroepiandrosteroneJennifer L.J. Heaney, Anna C. Phillips, Douglas Carroll10.1016/j.psyneuen.2011.07.001Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles341349http://www.psyneuen-journal.com/article/PIIS0306453011001892/abstract?rss=yesSummary: Background: Alterations in hypothalamic–pituitary–adrenal (HPA) axis activity have been observed in Gulf War veterans with posttraumatic stress disorder (PTSD) which differ from those observed in other veteran groups, raising the possibility that there is a unique neuroendocrine profile in this group of veterans. This study seeks to further characterize the effects of PTSD, military cohort (Vietnam, 1991 Gulf War, Operations Enduring Freedom/Iraqi Freedom (OEF/OIF)), and their interaction on the neuroendocrine response to synthetic corticotrophin-releasing factor (CRF) stimulation.Methods: 51 male veterans were studied consisting of 21 from the Vietnam era, 16 from the Gulf War era, and 14 from the OEF/OIF era. 16 of these veterans were deployed to a war zone and had chronic PTSD (PTSD+), 25 were deployed to a war zone and did not have chronic PTSD (PTSD−), and 10 were not deployed to a war zone and did not have PTSD (non-exposed). The participants underwent the CRF stimulation test in the afternoon (approximately 2:00 p.m.), which measures the integrity and sensitivity of the pituitary–adrenal axis. Plasma cortisol and adrenocorticotropic hormone (ACTH) were measured at baseline and at intervals over a 2h period following intravenous administration of 1μg/kg of ovine CRF (o-CRF, max 100μg). In a small subset of participants, dehydroepiandrosterone (DHEA) and cortisol binding globulin (CBG) were also assessed.Results: There was a significant group by era interaction in the response of ACTH to CRF, in addition to a main effect of group (PTSD+, PTSD−, non-exposed). The interaction reflected that group differences were only evident in the Gulf War cohort; among Gulf War era veterans, the PTSD+ group had higher elevations in ACTH levels following CRF than the PTSD− group and the non-exposed group. Additionally, the peak change in ACTH was associated with a self-reported environmental exposure (pyridostigmine bromide ingestion) which has been found to be linked to the excess morbidity found in Gulf War veterans. Self-reported childhood trauma was greater in veterans of the Gulf War than Vietnam or OEF/OIF, but did not account for the observed differences. There was a significant effect of group on the cortisol response to CRF, reflecting greater responsivity in both of the deployed groups (PTSD+ and PTSD−) compared to the non-exposed group which could be accounted for by baseline differences in cortisol levels; unlike the ACTH response, the cortisol response did not differ by era. There were no effects of group, era, or their interaction on the DHEA and CBG response to CRF.Conclusions: A uniform pattern of PTSD-related alterations in the response to intravenous CRF was not found. Rather, PTSD-related alterations were found only in veterans of the 1991 Gulf War, and were characterized by an enhanced pituitary response to CRF which may reflect increased sensitivity of pituitary corticotrophs or CRF hyposecretion. Together with previous neuroendocrine findings, the data suggest the HPA axis is dysregulated in Gulf War veterans in unique ways which may reflect the long-term effects of environmental exposures in addition to disease effects. Further work is needed to characterize these effects and their impact on long-term psychological and medical outcomes.Neuroendocrine response to CRF stimulation in veterans with and without PTSD in consideration of war zone eraJulia A. Golier, Kimberly Caramanica, Rachel Yehuda10.1016/j.psyneuen.2011.07.004Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles350357http://www.psyneuen-journal.com/article/PIIS0306453011001909/abstract?rss=yesSummary: Metabolic and cognitive disorders are closely related. However, the molecular mechanism underlying this association is still elusive. Given the importance of energy metabolism in neuronal cells, AMP-activated protein kinase (AMPK), a master switch of energy metabolism, could be an independent factor affecting cognitive as well as metabolic functions. Therefore, we examined the relationship between the AMPK γ2 gene, the PRKAG2 −26C/T polymorphism and cognitive impairment or diabetes in 1609 subjects aged from 60 to 80. We performed multivariate logistic regression analyses with adjustment for age, gender, education, smoking, alcohol, depression, waist circumference, APOE e4, and stroke history. We found a significant association between the −26C/T polymorphism (CC vs. CT/TT) and cognitive impairment (OR, 1.6; 95% CI, 1.1–2.3). Moreover, this polymorphism (CC/CT vs. TT) was also related to the presence of diabetes (OR, 1.8; 95% CI, 1.2–2.8). Importantly, the relationship with cognitive impairment was still significant in non-diabetic individuals (OR, 1.6; 95% CI, 1.1–2.4). Further analyses with a subpopulation (n=611) revealed that CC homozygotes relative to T-allele carriers had significantly better performances in verbal memory and attentional tasks. These findings collectively support a hypothesis that AMPK has a role not only in metabolic functioning but also in cognitive functioning in humans. Extended longitudinal study with a larger number of samples is warranted.AMPK γ2 subunit gene PRKAG2 polymorphism associated with cognitive impairment as well as diabetes in old ageEosu Kim, Sung Hee Lee, Kang Soo Lee, Hae-Kwan Cheong, Kee Namkoong, Chang Hyung Hong, Byoung Hoon Oh10.1016/j.psyneuen.2011.07.005Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles358365http://www.psyneuen-journal.com/article/PIIS0306453011001910/abstract?rss=yesSummary: Abnormalities of the hypothalamic–pituitary–adrenal (HPA) axis have been reported in subjects with Alzheimer's disease (AD) and may include increased cerebrospinal fluid (CSF) cortisol concentrations. Moreover, presence of the APOE ɛ4 allele, which is an established risk factor for the development of AD, has been shown to associate with higher CSF cortisol levels, especially in AD sufferers. In this study, we examined whether TOMM40 variants, which have been reported to influence age of onset of AD, also had an effect on CSF cortisol levels, in healthy, cognitively intact individuals with or without APOE ɛ4. In our results, the increase in CSF cortisol associated with the presence of the APOE ɛ4 allele was only detected when a short TOMM40 poly-T variant, shown to associate with later age of onset of AD in ɛ4 carriers, was not present. These results are consistent with previous reports (e.g., ) suggesting that TOMM40 poly-T variants influence the effects of APOE alleles.Cerebrospinal fluid cortisol concentrations in healthy elderly are affected by both APOE and TOMM40 variantsDavide Bruno, Jay J. Nierenberg, James C. Ritchie, Michael W. Lutz, Nunzio Pomara10.1016/j.psyneuen.2011.07.006Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles366371http://www.psyneuen-journal.com/article/PIIS0306453011001922/abstract?rss=yesSummary: While cognitive changes and mood instability are frequent symptoms reported by menopausal women, the degree to which the decline in estrogen production is responsible is not yet clear. Several lines of evidence suggest that estrogen may produce its effects on cognition and mood through modulation of serotonergic function. To test this hypothesis, we used the tryptophan depletion (TD) paradigm to lower central serotonin levels and pharmacologically manipulated estrogen levels in healthy menopausal women. We examined the individual and combined effects of estradiol and serotonin on working memory, emotion processing and task-related brain activation. Eight healthy predominantly early postmenopausal women underwent TD or sham depletion followed by functional magnetic resonance imaging (fMRI) both before and after short-term transdermal estradiol 75–150μg/d administration. There was an estradiol treatment by TD interaction for brain activation during performance on both the N-back Task (working memory) and Emotion Identification Task (affective processing). During the 2-back condition, TD attenuated activation prior to, but not after, estradiol treatment in the right and left dorsal lateral prefrontal and middle frontal/cingulate gyrus. During emotion identification, TD heightened activation in the orbital frontal cortex and bilateral amygdala, and this effect was attenuated by estradiol treatment. These results provide preliminary evidence that serotonergic effects directly mediate the impact of estrogen on brain activation during working memory and affective processing.Interactive effects of estrogen and serotonin on brain activation during working memory and affective processing in menopausal womenC. Neill Epperson, Zenab Amin, Kosha Ruparel, Ruben Gur, James Loughead10.1016/j.psyneuen.2011.07.007Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles372382http://www.psyneuen-journal.com/article/PIIS0306453011001946/abstract?rss=yesSummary: Many sex differences can be found in the expression of aggression and parental nurturing behaviors. It is important to determine if these are modulated by prenatal conditions. Here, using assisted reproduction technologies, we generated females that were (mixed-sex) or were not (same-sex) exposed to males during fetal development, raised them by cross fostering among fosters’ own female only pups to control for effects of postnatal environment, and compared their reproductive abilities and behavior. There were no differences between females from the two prenatal conditions in estrus cycle length and length of time spent at individual estrus cycle stages. Both types of females had similar ovulation efficiency and bred equally well yielding comparable litter size and progeny sex ratio. Females from the two prenatal conditions were also indistinguishable in social behavior and exhibited normal social responses towards unfamiliar females in the three-chamber social approach and social proximity tests. When urine was collected from both types of females and used as a point source in a scent-marking paradigm, exposed males showed a similar distribution and extent of urinary scent marking in response to urine from each type of female but tended to engage in higher durations of sniffing the urine from same-sex females. When females were tested in a resident-intruder paradigm 3 days after giving birth, same-sex females exhibited enhancement of pup grooming and an overall decrease of non-pup activity prior to male intruder introduction, and after introduction were more defensive as evidenced by higher rates of burying, open-mouth threat/lunges, and attacks towards the male, and decreased latencies to display these defensive behaviors. Our results suggest that females devoid of male exposure during fetal development have reproductive abilities similar to those of females from mixed-sex pregnancies, and have normal social interactions with other females. However, they exhibit hyper-maternal behavior both in terms of the care and defense of pups in front of a male intruder, and potentially produce a pheromonal milieu that renders them more attractive to males during olfactory investigations.Mouse females devoid of exposure to males during fetal development exhibit increased maternal behaviorAtsushi Sugawara, Brandon L. Pearson, D. Caroline Blanchard, Monika A. Ward10.1016/j.psyneuen.2011.07.009Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles383395http://www.psyneuen-journal.com/article/PIIS0306453011002071/abstract?rss=yesSummary: Increasing evidence in humans and other animals suggests that testosterone (T) plays an important role in modulating emotion. We previously reported that T treatment in rhesus monkeys undergoing chemically induced hypogonadism results in increased watching time of videos depicting fights between unfamiliar conspecifics (). In the current study, we aimed to further investigate the effect of T manipulations on attention and memory for emotional stimuli in male rhesus monkeys. Six males (7 years old) were administered Depot Lupron to suppress endogenous T levels and treated with either testosterone enanthate (TE, 5mg/kg) or oil, before crossing over to the alternate treatment. Animals were tested for 16 weeks on two computerized touchscreen tasks with both social and nonsocial emotional and neutral stimuli. The Dot-Probe task was used to measure attention, and the Delayed-Non-Matching-to-Sample task with a 1s delay (DNMS) was used to measure recognition memory for these stimuli. Performance on the two tasks was examined during each of four month-long phases: Baseline, Lupron alone, Lupron+TE and Lupron+oil. It was predicted that T administration would lead to increased attention to negative social stimuli (i.e., negative facial expressions of unfamiliar conspecifics) and would improve memory for such stimuli. We found no evidence to support these predictions. In the Dot-Probe task, an attentional bias towards negative social stimuli was observed at baseline, but T treatment did not enhance this bias. Instead, monkeys had faster response times when treated with T compared to oil, independently of the emotional valence or social relevance of stimuli, perhaps reflecting an enhancing effect of T on reward sensitivity or general arousal. In the DNMS, animals had better memory for nonsocial compared to social stimuli and showed the poorest performance in the recognition of positive facial expressions. However, T did not affect performance on the task. Thus, even though monkeys were sensitive to the social relevance and emotional valence of the stimuli in the two tasks, T manipulations had no effect on attention or memory for these stimuli. Because habituation to the stimuli may have mitigated the effect of treatment in the attentional task, we suggest that T may increase attentional biases to negative social stimuli only during early exposure to the stimuli with acute treatment or when stimuli are highly arousing (i.e., dynamically presented) with chronic treatment. In addition, the data suggest that T does not enhance working memory for emotional stimuli in young male macaques.Effects of testosterone on attention and memory for emotional stimuli in male rhesus monkeysHanna M. King, Laura B. Kurdziel, Jerrold S. Meyer, Agnès Lacreuse10.1016/j.psyneuen.2011.07.010Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles396409http://www.psyneuen-journal.com/article/PIIS0306453011002095/abstract?rss=yesSummary: Although not directly evaluated, the early rise of glucocorticoid (GC) levels, as occur after exposure to adverse early life experience, are assumed to affect hippocampal ontogeny by altering the hippocampus negative feedback on adult HPA axis. To test whether hippocampal ontogeny is affected by early exposure to stress we estimated the survival of recently formed hippocampal granule cells in rat pups subjected to periodic maternal separation (180min/day; MS180) from postnatal days (PND) 1 to 14. Accordingly, MS180 pups injected with bromodeoxyuridine (BrdU, 50mg/kg, ip) at PND 5 showed decreased density of doublecortin (DCX) positive BrdU-labeled cells at PND 15. MS180 and AFR pups showed similar corticosterone (CORT) basal levels between PND 3 and 12, whereas adult MS180 rats presented with higher CORT levels than AFR adults. Nonetheless, both AFR and MS180 pups and adults showed similar transient increments of CORT levels in response to stress. In addition, MS180 had no effect on the adult anxiety-like behavior evaluated in the elevated plus maze, but evoked a passive coping strategy in the forced swimming test. The data show that the decrease in hippocampal neurogenesis is an early onset phenomenon, and suggests that adverse experiences alter hippocampal ontogeny without chronic elevation of GC levels.Periodic maternal separation decreases hippocampal neurogenesis without affecting basal corticosterone during the stress hyporesponsive period, but alters HPA axis and coping behavior in adulthoodNaima Lajud, Angélica Roque, Marco Cajero, Gabriel Gutiérrez-Ospina, Luz Torner10.1016/j.psyneuen.2011.07.011Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles410420http://www.psyneuen-journal.com/article/PIIS0306453011002101/abstract?rss=yesSummary: Potent glucocorticoids (GC) administered early in life have improved premature infant survival dramatically. However, these agents may increase the risk for physical, neurological and behavior alterations. Anxiety, depression and attention difficulties are commonly described in adolescent and young adult survivors of prematurity. In the present study we administered vehicle, dexamethasone, or hydrocortisone to Sprague-Dawley rat pups on postnatal days 5 and 6, mimicking a short term clinical protocol commonly used in human infants. Two systems that are implicated in the regulation of stress and behavior were assessed: the limbic–hypothalamic–pituitary–adrenal axis [LHPA; glucocorticoid and mineralocorticoid receptors within] and the Serotonin (5-HT) system. We found that as adults, male Sprague-Dawley pups treated with GC showed agent specific altered growth, anxiety-related behavior, changes in corticoid response to novelty and gene expression changes within LHPA and 5-HT-related circuitry. The data suggest that prolonged GC-receptor stimulation during the early neonatal period can contribute to the development of individual differences in stress response and anxiety-related behavior later in life.Regulation of corticoid and serotonin receptor brain system following early life exposure of glucocorticoids: Long term implications for the neurobiology of moodDelia M. Vázquez, Charles R. Neal, Paresh D. Patel, Niko Kaciroti, Juan F. López10.1016/j.psyneuen.2011.07.012Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Articles421437http://www.psyneuen-journal.com/article/PIIS0306453011001934/abstract?rss=yesSummary: The neuropeptide oxytocin has a popular reputation of being the ‘love’ hormone. Here we test meta-analytically whether experiments with intranasal administration of oxytocin provide support for the proposed effects of oxytocin. Three psychological effects were subjected to meta-analysis: facial emotion recognition (13 effect sizes, N=408), in-group trust (8 effect sizes, N=317), and out-group trust (10 effect sizes; N=505). We found that intranasal oxytocin administration enhances the recognition of facial expressions of emotions, and that it elevates the level of in-group trust. The hypothesis that out-group trust is significantly decreased in the oxytocin condition was not supported. It is concluded that a sniff of oxytocin can change emotion perception and behavior in trusting relationships.A sniff of trust: Meta-analysis of the effects of intranasal oxytocin administration on face recognition, trust to in-group, and trust to out-groupMarinus H. Van IJzendoorn, Marian J. Bakermans-Kranenburg10.1016/j.psyneuen.2011.07.008Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Short Communication438443http://www.psyneuen-journal.com/article/PIIS0306453011003660/abstract?rss=yesNonapeptides (vasopressin, oxytocin, and homologues) broadly influence vertebrate social behavior, and the functions of nonapeptides and sex steroid hormones are extensively intertwined. In an effort to synthesize the nonapeptide and hormone literatures, van Anders et al. (2011, Psychoneuroendocrinology 36: 1365–1375) recently proposed a “steroid/peptide theory of social bonding.” This ambitious undertaking included the proposition of a model that predicts the release of nonapeptides and testosterone in relation to a variety of stimuli, and predicts the downstream effects on social bonding.Nonapeptides are not just for bonding: A response to van Anders et al. (2011)James L. Goodson10.1016/j.psyneuen.2011.12.011Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Correspondence444445http://www.psyneuen-journal.com/article/PIIS0306453011003672/abstract?rss=yesWe welcome Dr. Goodson's response to our Steroid/Peptide (S/P) Theory of Social Bonds (2011, Psychoneuroendocrinology 36, 1365–1375) and appreciate the venue for additional discussion. We hope to clarify possible misreadings and foster dialogue about our differing levels of analysis.The steroid/peptide theory of social bonds: A reply to Goodson's Letter to the EditorSari M. van Anders, Katherine L. Goldey10.1016/j.psyneuen.2011.12.012Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Correspondence445445http://www.psyneuen-journal.com/article/PIIS0306453011003611/abstract?rss=yesThe publisher regrets that A. Leslie Morrow, United States, was accidentally omitted from the list of reviewers. The publisher would like to apologise for any inconvenience caused.Erratum to “Acknowledgement to Reviewers” [Psychoneuroendocrinology 37 (2012) I–VI]10.1016/j.psyneuen.2011.12.006Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7Erratum446446http://www.psyneuen-journal.com/article/PIIS0306453012000170/abstract?rss=yes2012 Curt P. Richter Award of the International Society of Psychoneuroendocrinology (ISPNE)10.1016/S0306-4530(12)00017-0Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7IIhttp://www.psyneuen-journal.com/article/PIIS0306453012000182/abstract?rss=yesISPNE Conference Announcement10.1016/S0306-4530(12)00018-2Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7IIIIhttp://www.psyneuen-journal.com/article/PIIS0306453012000194/abstract?rss=yesISPNE Call for Abstracts10.1016/S0306-4530(12)00019-4Psychoneuroendocrinology 37, 3 (2012)2012-03-01Psychoneuroendocrinology2012-03-01373S0306-4530(12)X0002-7IIIIII