Hormonal and experiential predictors of infant survivorship and maternal behavior in a monogamous primate (Callicebus cupreus).

To better understand the roles that hormones and experience play in infant survival and maternal behavior in a biparental primate species, we analyzed urinary estrone (E(1)C) and pregnanediol glucuronide (PdG) from 24 socially housed titi monkey (Callicebus cupreus) females over 54 pregnancies (N = 1,430 samples). Pregnancies were categorized according to whether the infant survived (N = 35) or not (N = 19), and by maternal parity (primiparous: N = 9; multiparous: N = 45). Mothers of infants that survived had a significantly greater drop in PdG from the third trimester to the first week postpartum than mothers of infants that did not survive. Multiparous mothers had a greater increase in PdG from the first to the third trimester as well as greater increases in the E(1)C:PdG ratio from the first to the third trimester and from the third trimester to the first week postpartum. There were positive relationships between third trimester PdG and maternal carrying and nursing during the first week postpartum, and between maternal age and carrying during the infant's first month of life. There was a negative correlation between maternal age and PdG during the third trimester. These results suggest that elevated progesterone during late pregnancy followed by progesterone withdrawal immediately following parturition is associated with greater probability of infant survivorship and maternal behavior in this species, and that older females engage in more postpartum maternal care

Hormonal and experiential predictors of infant survivorship and maternal behavior in a monogamous primate (Callicebus cupreus).

To better understand the roles that hormones and experience play in infant survival and maternal behavior in a biparental primate species, we analyzed urinary estrone (E(1)C) and pregnanediol glucuronide (PdG) from 24 socially housed titi monkey (Callicebus cupreus) females over 54 pregnancies (N = 1,430 samples). Pregnancies were categorized according to whether the infant survived (N = 35) or not (N = 19), and by maternal parity (primiparous: N = 9; multiparous: N = 45). Mothers of infants that survived had a significantly greater drop in PdG from the third trimester to the first week postpartum than mothers of infants that did not survive. Multiparous mothers had a greater increase in PdG from the first to the third trimester as well as greater increases in the E(1)C:PdG ratio from the first to the third trimester and from the third trimester to the first week postpartum. There were positive relationships between third trimester PdG and maternal carrying and nursing during the first week postpartum, and between maternal age and carrying during the infant's first month of life. There was a negative correlation between maternal age and PdG during the third trimester. These results suggest that elevated progesterone during late pregnancy followed by progesterone withdrawal immediately following parturition is associated with greater probability of infant survivorship and maternal behavior in this species, and that older females engage in more postpartum maternal care

Presence of a pair-mate regulates the behavioral and physiological effects of opioid manipulation in the monogamous titi monkey (Callicebus cupreus).

The role of opioid receptors in infant-mother attachment has been well established. Morphine, a preferential μ opioid receptor (MOR) agonist, attenuates separation distress vocalizations and decreases physical contact between infant and mother. However, there is little research on how opioid receptors are involved in adult attachment. The present study used the monogamous titi monkey (Callicebus cupreus) to explore the role of opioid receptors in the behavioral and physiological components of pair-bonding. In Experiment 1, paired male titi monkeys (N=8) received morphine (0.1, 0.5, or 1.0mg/kg), the opioid antagonist naloxone (1.0mg/kg), vehicle, or a disturbance control and were filmed with their pair-mate for 1h. In Experiment 2, the same eight males received morphine (0.25mg/kg), naloxone (1.0mg/kg), vehicle, or a disturbance control and were filmed for an hour without their pair-mates. All video sessions were scored for social and non-social behaviors. Blood was sampled immediately prior to drug administration and at the end of the hour session. Plasma was assayed for cortisol, oxytocin, and vasopressin. In Experiment 1, opioid manipulation had no effect on affiliative behaviors; however, morphine dose-dependently decreased locomotor behavior and increased scratching. In Experiment 2 in which males were separated from their pair-mates, naloxone increased locomotion. Morphine dose-dependently attenuated the rise in cortisol, while naloxone potentiated the increase of cortisol. The cortisol increase following naloxone administration was greater when a male was alone compared to when the male was with his pair-mate. Naloxone increased vasopressin but only when the male was tested without his pair-mate. The present study found that the absence of a pair-mate magnified naloxone's effects on stress-related hormones and behaviors, suggesting that the presence of a pair-mate can act as a social buffer against the stress-inducing effects of naloxone

Presence of a pair-mate regulates the behavioral and physiological effects of opioid manipulation in the monogamous titi monkey (Callicebus cupreus).

The role of opioid receptors in infant-mother attachment has been well established. Morphine, a preferential μ opioid receptor (MOR) agonist, attenuates separation distress vocalizations and decreases physical contact between infant and mother. However, there is little research on how opioid receptors are involved in adult attachment. The present study used the monogamous titi monkey (Callicebus cupreus) to explore the role of opioid receptors in the behavioral and physiological components of pair-bonding. In Experiment 1, paired male titi monkeys (N=8) received morphine (0.1, 0.5, or 1.0mg/kg), the opioid antagonist naloxone (1.0mg/kg), vehicle, or a disturbance control and were filmed with their pair-mate for 1h. In Experiment 2, the same eight males received morphine (0.25mg/kg), naloxone (1.0mg/kg), vehicle, or a disturbance control and were filmed for an hour without their pair-mates. All video sessions were scored for social and non-social behaviors. Blood was sampled immediately prior to drug administration and at the end of the hour session. Plasma was assayed for cortisol, oxytocin, and vasopressin. In Experiment 1, opioid manipulation had no effect on affiliative behaviors; however, morphine dose-dependently decreased locomotor behavior and increased scratching. In Experiment 2 in which males were separated from their pair-mates, naloxone increased locomotion. Morphine dose-dependently attenuated the rise in cortisol, while naloxone potentiated the increase of cortisol. The cortisol increase following naloxone administration was greater when a male was alone compared to when the male was with his pair-mate. Naloxone increased vasopressin but only when the male was tested without his pair-mate. The present study found that the absence of a pair-mate magnified naloxone's effects on stress-related hormones and behaviors, suggesting that the presence of a pair-mate can act as a social buffer against the stress-inducing effects of naloxone

Dysregulated diurnal cortisol pattern is associated with glucocorticoid resistance in women with major depressive disorder

Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is believed to play a role in the pathophysiology of depression. To investigate mechanisms that may underlie this effect, we examined several indices of HPA axis function - specifically, diurnal cortisol slope, cortisol awakening response, and suppression of cortisol release following dexamethasone administration - in 26 pre-menopausal depressed women and 23 never depressed women who were matched for age and body mass index. Salivary cortisol samples were collected at waking, 30 min after waking, and at bedtime over three consecutive days. On the third day, immediately after the bedtime sample, participants ingested a 0.5mg dexamethasone tablet; they then collected cortisol samples at waking and 30 min after waking the following morning. As predicted, depressed women exhibited flatter diurnal cortisol rhythms and more impaired suppression of cortisol following dexamethasone administration than non-depressed women over the three sampling days. In addition, flatter diurnal cortisol slopes were associated with reduced cortisol response to dexamethasone treatment, both for all women and for depressed women when considered separately. Finally, greater self-reported depression severity was associated with flatter diurnal cortisol slopes and with less dexamethasone-related cortisol suppression for depressed women. Depression in women thus appears to be characterized by altered HPA axis functioning, as indexed by flatter diurnal cortisol slopes and an associated impaired sensitivity of cortisol to dexamethasone. Given that altered HPA axis functioning has been implicated in several somatic conditions, the present findings may be relevant for understanding the pathophysiology of both depression and depression-related physical disease

Greater amygdala activity and dorsomedial prefrontal-amygdala coupling are associated with enhanced inflammatory responses to stress.

Psychological stress is implicated in the etiology of many common chronic diseases and mental health disorders. Recent research suggests that inflammation may be a key biological mediator linking stress and health. Nevertheless, the neurocognitive pathways underlying stress-related increases in inflammatory activity are largely unknown. The present study thus examined associations between neural and inflammatory responses to an acute laboratory-based social stressor. Healthy female participants (n=31) were exposed to a brief episode of stress while they underwent an fMRI scan. Blood samples were taken before and after the stressor, and plasma was assayed for markers of inflammatory activity. Exposure to the stressor was associated with significant increases in feelings of social evaluation and rejection, and with increases in levels of inflammation. Analyses linking the neural and inflammatory data revealed that heightened neural activity in the amygdala in response to the stressor was associated with greater increases in inflammation. Functional connectivity analyses indicated that individuals who showed stronger coupling between the amygdala and the dorsomedial prefrontal cortex (DMPFC) also showed a heightened inflammatory response to the stressor. Interestingly, activity in a different set of neural regions was related to increases in feelings of social rejection. These data show that greater amygdala activity in response to a stressor, as well as tighter coupling between the amygdala and the DMPFC, are associated with greater increases in inflammatory activity. Results from this study begin to identify neural mechanisms that might link stress with increased risk for inflammation-related disorders such as cardiovascular disease and depression