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HPA Regulation (hpa + regulation)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Rearing environment and hypothalamic-pituitary-adrenal regulation in young rhesus monkeys (Macaca mulatta)

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 4 2005
John P. Capitanio
Abstract A mammal's early social environment has important regulatory effects on its behavior and physiology, and this is especially true for regulation of the hypothalamic-pituitary-adrenal (HPA) system. The present study was designed to test hypotheses that various aspects of the social environment are important influences on HPA regulation. Seven hundred seventy eight, 3- to 4-month-old rhesus monkeys were studied as part of a standardized, 24-hr biobehavioral assessment program, which included blood sampling to determine plasma cortisol concentrations. Results indicate that nursery-rearing results in a reduced cortisol set-point for the HPA system, and, for nursery-reared (NR) animals, more peer exposure during infancy is associated with a higher set-point. Age and sex differences during this period were evident but small in magnitude. These data demonstrate the important regulatory role of the social environment on nonhuman primate physiology and suggest caution in assuming that differences between individuals' cortisol levels reflect only differences in perceptions of the "stressfulness" of events. © 2005 Wiley Periodicals, Inc. Dev Psychobiol 46:318,330, 2005. [source]

Hypothalamic-pituitary-adrenal axis activation by experimental periodontal disease in rats

JOURNAL OF PERIODONTAL RESEARCH, Issue 5 2001
T. Breivik
Organisms respond to inflammatory conditions by mounting a co-ordinated complex series of adaptive responses involving the immune, nervous and endocrine systems that are aimed at restoring the homeostatic balance. We have recently shown in a rat model that inappropriate hypothalamic-pituitary-adrenal (HPA) axis regulation and a subsequent inability to mount a suitable glucocorticoid response to gingival inflammation may influence susceptibility to periodontal disease. This study was designed to investigate whether ligature- and bacterial lipopolysaccharide (LPS)-induced inflammation in the gingival connective tissues may activate this physiological axis, and to further explore the significance of HPA regulation in periodontal disease. Experimental periodontal disease was induced in major histocompability complex (MHC)-identical but HPA low (LEW) and high (F344) responding rat strains. We tested (1) whether ongoing periodontal disease activates the HPA axis as measured by corticosterone levels, and (2) whether genetic differences in HPA regulation modulate periodontal disease progression. In the F344 strain, the periodontal tissue destruction was more severe. This observation was associated with a significant increase of corticosterone levels in F344 rats only. Addition of LPS at the gingival inflammatory site led to a further increase of corticosterone levels and disease severity in F344 rats. These findings illustrate a positive feedback loop between the HPA axis and periodontal disease: the disease activates the HPA axis, and a genetically determined high HPA responsitivity further increases disease susceptibility. [source]

Effects of Prenatal Ethanol Exposure on Hypothalamic-Pituitary-Adrenal Function Across the Estrous Cycle

ALCOHOLISM, Issue 6 2009
Ni 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]

Are cortisol profiles a stable trait during child development?

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 6 2009
Mark V. Flinn
Exposure to stressful experiences can increase vulnerability to adverse health outcomes. A potential neuroendocrine mechanism mediating the link between stress and health is the hypothalamic-pituitary-adrenal (HPA) system, with a key role attributed to the glucocorticoid hormone cortisol. Retrospective and cross sectional clinical studies of humans and experimental studies with nonhuman primates and rodents suggest that traumatic experiences during critical periods in development may have permanent effects on HPA regulation, which in turn can have deleterious effects on health. Here I report results from a continuous 20-year study (1988,2009) of children in a rural community on Dominica. Sequential data on cortisol levels, social stressors, and health in naturalistic, everyday conditions are examined to assess developmental trajectories of HPA functioning. Saliva aliquots were assayed for cortisol in concert with monitoring of growth, morbidity, and social environment. Analyses here include data from 1989 to 1999 for 147 children aged 3,16 years with >100 saliva samples each. Cortisol values were standardized by elapsed time since wake-up. Results do not support the hypothesis that traumatic stress during childhood causes permanent general elevation of cortisol levels. Am. J. Hum. Biol., 2009. © 2009 Wiley-Liss, Inc. [source]