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HPA Activity (hpa + activity)
Selected AbstractsStress reactivity: biological and subjective responses to the cold pressor and Trier Social stressors,HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 6 2006Aimee L. McRae Abstract The cold pressor test (CPT) and Trier Social Stress Test (TSST) have been shown to reliably increase HPA activity; however, little research has compared responses to these stressors. In this study, biological (plasma cortisol and ACTH levels) and subjective (e.g., stress and mood) responses were compared in 31 subjects administered both the CPT and TSST. Subjects were diagnosed with alcohol dependence and post-traumatic stress disorder (PTSD) (n,=,11), alcohol dependence without PTSD (n,=,10), PTSD without alcohol use disorder (n,=,4), and neither PTSD nor alcohol use disorder (n,=,6). All subjects completed both the CPT and TSST. In all groups, the TSST elicited higher levels of ACTH and cortisol than the CPT, and the response time course differed between tasks. The TSST also produced lower mood ratings than the CPT. A comparison of all diagnosed groups with normal controls revealed group differences in ACTH responding for the CPT but not the TSST. The results suggest that the TSST results in a greater HPA response than the CPT; however, the CPT may have utility in diagnostically heterogeneous patients. Copyright © 2006 John Wiley & Sons, Ltd. [source] Hypothalamic-Pituitary-Adrenal Axis Abnormalities in Response to Deletion of 11,-HSD1 is Strain-DependentJOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2009R. N. Carter Inter-individual differences in hypothalamic-pituitary-adrenal (HPA) axis activity underlie differential vulnerability to neuropsychiatric and metabolic disorders, although the basis of this variation is poorly understood. 11,-Hydroxysteroid dehydrogenase type 1 (11,-HSD1) has previously been shown to influence HPA axis activity. 129/MF1 mice null for 11,-HSD1 (129/MF1 HSD1,/,) have greatly increased adrenal gland size and altered HPA activity, consistent with reduced glucocorticoid negative feedback. On this background, concentrations of plasma corticosterone and adrenocorticotrophic hormone (ACTH) were elevated in unstressed mice, and showed a delayed return to baseline after stress in HSD1-null mice with reduced sensitivity to exogenous glucocorticoid feedback compared to same-background genetic controls. In the present study, we report that the genetic background can dramatically alter this pattern. By contrast to HSD1,/, mice on a 129/MF1 background, HSD1,/, mice congenic on a C57Bl/6J background have normal basal plasma corticosterone and ACTH concentrations and exhibit normal return to baseline of plasma corticosterone and ACTH concentrations after stress. Furthermore, in contrast to 129/MF1 HSD1,/, mice, C57Bl/6J HSD1,/, mice have increased glucocorticoid receptor expression in areas of the brain involved in glucocorticoid negative feedback (hippocampus and paraventricular nucleus), suggesting this may be a compensatory response to normalise feedback control of the HPA axis. In support of this hypothesis, C57Bl/6J HSD1,/, mice show increased sensitivity to dexamethasone-mediated suppression of peak corticosterone. Thus, although 11,-HSD1 appears to contribute to regulation of the HPA axis, the genetic background is crucial in governing the response to (and hence the consequences of) its loss. Similar variations in plasticity may underpin inter-individual differences in vulnerability to disorders associated with HPA axis dysregulation. They also indicate that 11,-HSD1 inhibition does not inevitably activate the HPA axis. [source] Changes in Hypothalamic-Pituitary-Adrenal Function, Body Temperature, Body Weight and Food Intake with Repeated Social Stress Exposure in RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2006S. Bhatnagar Abstract These present studies aimed to compare changes in hypothalamic-pituitary-adrenal (HPA) activity and body temperature in response to acute social defeat, to repeated social stress and to novel restraint after repeated stress, as well as to assess effects on metabolic parameters by measuring body weight gain and food and water intake. We found that social defeat produced a marked increase in both adrenocorticotrophic hormone and corticosterone compared to placement in a novel cage. Similarly, body temperature was also increased during social defeat and during 30 min of recovery from defeat. We then examined the effects of 6 days of repeated social stress and observed minimal HPA responses to repeated social stress compared to control rats. These neuroendocrine responses were contrasted by robust increases in body temperature during stress and during recovery from stress during 6 days of repeated stress. However, in response to novel restraint, repeatedly stressed rats displayed facilitated body temperature responses compared to controls, similar to our previous findings with HPA activity. Food intake was increased during the light period during which defeat took place, but later intake during the dark period was not affected. Repeated stress decreased body weight gain in the dark period but food intake was increased overall during the 6 days of repeated stress in the light period. As a result, repeated stress increased cumulative food intake during the light period in the stressed rats but these relatively small increases in food intake were unable to prevent the diminished total weight gain in repeatedly stressed rats. Overall, the results demonstrate that, although acute social defeat has similar effects on temperature and HPA activity, repeated exposure to social stress has divergent effects on HPA activity compared to body temperature and that dampened weight gain produced by repeated social stress cannot be fully explained by changes in food intake. [source] Adrenocortical and Pituitary Glucocorticoid Feedback in Abstinent Alcohol-Dependent WomenALCOHOLISM, Issue 5 2010Bryon Adinoff Background:, The long-term ingestion of alcohol diminishes hypothalamic,pituitary,adrenal (HPA) axis reactivity in alcohol-dependent men, potentially altering future relapse risk. Although sex differences in HPA axis functioning are apparent in healthy controls, disruptions in this system have received little attention in alcohol-dependent women. In this study, we assessed the basal secretory profile of adrenocorticotropic hormone (ACTH) and cortisol, adrenocortical sensitivity in both the presence and absence of endogenous corticotropic pituitary activation, and feedback pituitary glucocorticoid sensitivity to dexamethasone. Methods:, Seven women 4- to 8-week abstinent alcohol-only dependent subjects and 10 age-matched female healthy controls were studied. All subjects were between 30 and 50 years old, not taking oral contraceptives, and were studied during the early follicular phase of their menstrual cycle. Circulating concentrations of ACTH and cortisol were measured in blood samples collected at frequent intervals from 2000 to 0800 hour. A submaximal dose of cosyntropin (0.01 ,g/kg), a synthetic ACTH (1,24), was administered at 0800 hour to assess adrenocortical sensitivity. In a separate session, low-dose cosyntropin was also administered following high-dose dexamethasone (8 mg intravenous) to assess adrenocortical sensitivity in the relative absence of endogenous ACTH. In addition, the ACTH response to dexamethasone was measured to determine the pituitary glucocorticoid negative feedback. Sessions were 5 days apart, and blood draws were obtained every 5 to 10 minutes. Results:, Mean concentrations and pulsatile characteristics of ACTH and cortisol over 12 hours were not statistically different between the 2 groups. Healthy controls had a somewhat higher (p < 0.08) net peak, but not net integrated, cortisol response to cosyntropin relative to the alcohol-dependent women. There were no significant group differences in either the ACTH or cortisol response to dexamethasone nor in the net cortisol response to cosyntropin following dexamethasone. Conclusion:, Significant differences in pituitary,adrenal function were not apparent between alcohol-dependent women and matched controls. Despite the small n, it appears that alcohol-dependent women do not show the same disruptions in HPA activity as alcohol-dependent men. These findings may have relevance for gender-specific treatment effectiveness. [source] Effects of Prenatal Ethanol Exposure on Hypothalamic-Pituitary-Adrenal Function Across the Estrous CycleALCOHOLISM, Issue 6 2009Ni Lan Background:, Rats prenatally exposed to ethanol (E) typically show increased hypothalamic-pituitary-adrenal (HPA) responses to stressors in adulthood. Importantly, prenatal ethanol may differentially alter stress responsiveness in male and female offspring, suggesting a role for the gonadal hormones in mediating the effects of ethanol on HPA activity. We investigated the role of ethanol-induced changes in hypothalamic-pituitary-gonadal (HPG) activity in the differential HPA regulation observed in E compared to control females across the estrous cycle. Methods:, Peripheral hormones and changes in central neuropeptide mRNA levels were measured across the estrous cycle in adult female offspring from E, pair-fed (PF) and ad libitum-fed control (C) dams. Results:, Ethanol females showed normal estrous cyclicity (vaginal smears) but delayed sexual maturation (vaginal opening). Both HPG and HPA activity were differentially altered in E (and in some cases, PF) compared to control females as a function of estrous cycle stage. In relation to HPG activity, E and PF females had higher basal and stress estradiol (E2) levels in proestrus compared to other phases of the cycle, and decreased GnRH mRNA levels compared to C females in diestrus. Further, E females had greater variation in LH than PF and C females across the cycle, and in proestrus, only E females showed a significant LH increase following stress. In relation to HPA activity, both basal and stress CORT levels and overall ACTH levels were greater in E than in C females in proestrus. Furthermore, AVP mRNA levels were increased overall in E compared to PF and C females. Conclusions:, These data demonstrate ethanol-induced changes in both HPG and HPA activity that are estrous phase-specific, and support the possibility that changes in HPA activity in E females may reflect differential sensitivity to ovarian steroids. E females appear to have an increased HPA sensitivity to E2, and a possible shift toward AVP regulation of HPA activity. That PF were similar to E females on some measures suggests that nutritional effects of diet or food restriction played a role in mediating at least some of the changes observed. [source] Gender- and Age-Related Differences in the Association Between Social Relationship Quality and Trait Levels of Salivary CortisolJOURNAL OF RESEARCH ON ADOLESCENCE, Issue 2 2008Alan Booth The majority of studies linking individual differences in the quality of social relationships and activity of the hypothalamic-pituitary-adrenal (HPA) axis have focused on the early development of attachment between infants and their caregivers. Later in development, during middle childhood and adolescence, the parallel HPA links to age-appropriate social relationships with peers, parents, and siblings remain largely unspecified. This study addressed this knowledge gap. Early morning saliva samples were obtained from 367 children in middle childhood (ages 6,10) and 357 adolescents (M age=11,16 years) on two successive days 1 year apart and assayed for cortisol. Latent state,trait modeling was employed to separate variance in cortisol levels attributable to "stable trait-like" versus "state or situational specific" sources to minimize the high moment-to-moment variation in basal adrenocortical activity. During adolescence but not middle childhood, and for girls but not boys, lower levels of "trait cortisol" were associated with poor quality social relationships. The pattern was robust, extending to the quality of relationships with parents, siblings, and peers. Importantly, the relationship was independent of the rates of internalizing or externalizing problem behavior. We found that isolating the variance in cortisol levels attributable to stable intrinsic sources revealed an interpretable pattern that linked individual differences in basal HPA activity to social relationships during adolescence. Studies are needed to reveal the biosocial mechanisms involved in the establishment of this gender- and age-specific phenomenon and to decipher whether or not individual differences in this hormone-behavior link are adaptive. [source] | ||||||||||