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1
Evuarherhe, Obaro. "Gender, puberty and the hypothalamic-pituitary-adrenal axis." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618813.
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The hypothalamo-pituitary-adrenal (HPA) axis, a neuroendocrine pathway involved in the stress response is well studied in both human beings and rodents. Major gender-related neuroendocrine changes take place during pubcl1y (days 30 - 60 in rats) including a robust increase in the levels of gonadal steroids which are thought to underlie numerous neural and behavioural changes brought on after puberty. Evidence suggests the HPA axis undergoes significant changes over the pubertal period. This project investigated the effects of gonadal steroids on the HPA axis before and after puberty and the role of the pubertal surge in endogenous gonadal steroids in both sexes; specifically looking at the sensitivity of the resulting adult HPA axis to exogenous gonadal steroids. There was a significant effect of both age and sex on the adrenocorticotrophic hormone (ACTH) and corticosterone response to restraint stress. Sexual dimorphism in the endocrine stress response became more pronounced after puberty. Adult physiological levels of gonadal steroids reduced the corticosterone and ACTH response to restraint stress in both male and female prepubertal rats. In adult males, testosterone reduced the ACTH response to stress while in adult females, there was a s significant effect of ovariectomy (OVX) on the stress response. 1:estosterone treatment did not significantly affect overall corticosterone release over the 24hr period in adult animals castrated (CSX) before puberty. In contrast, testosterone significantly suppressed corticosterone secretion in animals CSX in adulthood. Animals CSX prepubertally displayed significantly lower glucocorticoid receptor levels in the dentate gyrus of the dorsal hippocampus than animals CSX in adulthood. [n females, prepubertal OVX did not affect the ability of oestradiol to affect basal HPA activity in adulthood. Overall, the data suggest vital roles of peripubertal gonadal steroids on the adult HPA axis; although the pubertal maturation of the female HP A phenotype appears to be independent of peripubertal oestrogens.
2
Stirrat, Laura Ingram. "Hypothalamic pituitary adrenal axis dysregulation in obese pregnancy." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28979.
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There has been a global rise in obesity in the last three decades, and at present one in five women are obese at antenatal booking. Maternal obesity is associated with an increased risk of adverse pregnancy outcomes, including increased fetal size and prolonged pregnancy. In the longer-term, offspring of obese are at increased risk of premature death from a cardiovascular event in their adulthood. One mechanism that has been linked to these outcomes is fetal exposure to glucocorticoids in utero. During normal pregnancy, the maternal hypothalamic pituitary adrenal (HPA) axis undergoes major changes, resulting in exponentially increasing levels of the major circulating glucocorticoid cortisol, and other HPA axis hormones, such as corticotrophin releasing hormone (CRH). Cortisol and CRH are vital for normal fetal growth and length of gestation, but in excess they are associated with fetal growth restriction and preterm labour. In non-pregnant obesity, it is thought that the HPA axis is dysregulated, although evidence is inconclusive. Little is known about the effects of maternal obesity in pregnancy on the HPA axis. The work in this Thesis used clinical studies to test the hypothesis that the HPA axis is dysregulated in obese pregnant women with altered release, clearance and placental metabolism of cortisol. Associations with clinical outcomes related to fetal size and length of gestation were also studied. The HPA axis activity during pregnancy was investigated in a prospective case-control study cohort. Fasting serum cortisol levels were measured at 16, 28 and 36 weeks of gestation (obese n=276, lean n=135). In a subset (obese n=20, lean n=20), corticosteroid binding globulin (CBG), CRH, estrogens and progesterone were measured. Salivary cortisol was measured in samples collected at bedtime, waking and 30 minutes after waking at 16 weeks. Urinary glucocorticoid metabolites were measured at 19 weeks and 36 weeks (obese n=6, lean n=5) and non-pregnant (obese n=7, lean n=7) subjects. All circulating hormone levels rose similarly in obese and lean during pregnancy, but were significantly lower in obese women. The diurnal rhythm of cortisol was maintained. Urinary glucocorticoids increased with gestation in lean, but not in obese, indicating a lesser activation of the HPA axis in obese compared with lean pregnancy. These findings associated with increased birthweight and longer gestation in obese pregnancy, suggesting that decreased HPA axis activity may underlie these obese related adverse pregnancy outcomes. Whether or not lower glucocorticoids in obese pregnancies are maintained at delivery was investigated by measuring active glucocorticoids (cortisol and corticosterone) and their inactive versions (cortisone and 11- dehydrocorticosterone, respectively) from matched maternal and cord plasma samples (n=259, BMI 18 – 55 kg/m2). Active glucocorticoids were significantly higher in maternal than cord blood, and inactive versions were significantly higher in cord than maternal blood. Increased maternal BMI associated with lower maternal cortisol, corticosterone and 11-dehydrocorticosterone. Despite significant correlations between maternal and cord blood glucocorticoid levels, increased maternal BMI did not associate with lower cord blood glucocorticoids. This suggests that conditions at delivery may overcome any potential negative effects of low maternal glucocorticoids on the fetus in the short-term. However, it may not preclude the longer-term effects of fetal exposure to lower glucocorticoid levels during obese pregnancy, and offspring follow-up studies are required. Potential mechanisms leading to altered HPA axis activity in obese pregnancy were explored by studying the pulsatile release and placental metabolism of glucocorticoid hormones. Glucocorticoid pulsatility is thought to be important for transcriptional regulation of glucocorticoid responsive genes, and disruptions to pulsatility have been reported in some disease processes. Glucocorticoids were measured in 10-minute serum sampling between 08.00h-11.00h and 16.00h- 19.00h. Peripheral tissue cortisol was measured from 20-minute sampling of interstitial fluid, over 24-hours, at 16-24 weeks and 30-36 weeks (obese n=7, lean n=8), and non-pregnant controls (obese n=4, lean n=3). Total circulating serum cortisol levels were higher in pregnancy than non-pregnancy in lean and obese, and increased significantly with advancing gestation in lean but not in obese. Pulsatility of cortisol was demonstrated in interstitial fluid in both non-pregnancy and pregnancy. In obese pregnancy, interstitial fluid pulse frequency was lower with advancing gestation. This may be a novel mechanism underlying the observed decreased HPA axis activity in obese pregnancy. Placental cortisol metabolism and transport was studied using an ex vivo placental perfusion model, perfused with a deuterium-labelled cortisol tracer combined with computational modeling. The findings challenge the concept that maternal cortisol diffuses freely across the placenta, but confirmed that 11β- HSD2 acts as major ‘barrier’ to cortisol transfer to the fetus, protecting the fetus from the high maternal circulating cortisol levels. In addition we showed preliminary evidence of local cortisol production within the placenta. The model is able to predict maternal-fetal cortisol transfer and can now be used in future experimental design. In conclusion, in obese pregnancy, lower maternal cortisol and urinary clearance suggested reduced HPA axis activity. Altered glucocorticoid pulsatility may underlie this change. Future studies of placental cortisol metabolism in maternal obesity could be conducted using an ex vivo perfusion model. The lower HPA axis activity in obese pregnancy represents a novel pathway underlying increased fetal growth.
3
Näsman, Birgitta. "The limbic-hypothalamic-pituitary-adrenal axis in Alzheimer's disease." Doctoral thesis, Umeå universitet, Geriatrik, 1994. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-140822.
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Dysfunction of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis is a common finding in advanced dementia. In this study, the function of the LHPA axis at different levels was investigated in patients with dementia and in healthy elderly. A subtle disturbance in the feedback regulation of the LHPA axis was found in patients with early (i.e., mild to moderate) Alzheimer’s disease (AD). After 0.5 mg dexamethasone, serum cortisol levels were less suppressed in AD patients and plasma adrenocorticotropin (ACTH) levels were lower as compared with healthy elderly. After stimulation with human corticotropin-releasing hormone a blunted ACTH response was found in AD patients while relative serum cortisol, dehydroepiandrosterone, and androstenedione responses were increased. Significant correlations were found between low plasma ACTH levels and temporal lobe atrophy and between low peak plasma ACTH levels and hippocampal atrophy measured with computer tomography. Patients with advanced AD and multi-infarct dementia had lower basal levels of dehydroepiandrosterone sulphate in combination with no difference in cortisol levels, resulting in a high cortisol/DHAS ratio. The difference persisted after adjustments for age and sex in a multivariate analysis. In patients with early AD, basal serum levels of dehydroepiandrosterone and androstenedione were increased, and this increase was accentuated after stimulation with ACTH. Peripheral glucocorticoid sensitivity was examined by skin vasoconstrictor blanching tests. Patients with AD and patients treated with glucocorticoids showed skin blanching at higher clobetasol concentrations than healthy elderly. These findings justify further investigations on the role of LHPA axis dysfunction in Alzheimer’s disease and its possible importance for the pathophysiology of the disease.<br>digitalisering@umu
4
Watson, Stuart. "Hypothalamic-pituitary-adrenal axis function in mood disorder patients." Thesis, University of Newcastle upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413260.
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5
Dembek, Katarzyna Agnieszka. "Hypothalamic-pituitary-adrenal axis dysfunction in critically ill foals." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1479220019340433.
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6
Gillich, Anton. "The role of histamine in the hypothalamic - pituitary - adrenal axis /." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55496.
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Histamine appears to act as a neurotransmitter within the CNS and may be involved in the regulation of a number of physiological systems including the Hypothalamic-Pituitary-Adrenal (HPA) axis. We conducted a series of experiments in rats to examine the role of histamine within the HPA axis. We first determined if histamine undergoes diurnal variations in the paraventricular nucleus, the periventricular nucleus, and the ventro-medial nucleus of the hypothalamus, the frontal cortex, septal nucleus, median eminence, posterior hypothalamus, mammillary bodies, supraoptic nucleus, suprachiasmatic nucleus, bed nucleus of the stria terminalis, dentate gyrus, and the CA1, CA2, and CA3 cell fields of the hippocampus. We further examined the effect of adrenalectomy and corticosterone replacement in these areas to determine if the histaminergic system is susceptible to glucocorticoid negative feedback inhibition. Finally, histamine levels in the paraventricular hypothalamic nucleus, the periventricular nucleus, the median eminence, the posterior hypothalamus, the mammillary bodies, the supraoptic nucleus, and the suprachiasmatic nucleus were measured in rats that were either intact, adrenalectomized (ADX), or ADX and treated with corticosterone and were stressed for various periods of time.<br>The results suggest that (1) histamine may mediate basal plasma levels of ACTH through the regulation of paraventricular hypothalamic activity, (2) the histaminergic system may not be susceptible to glucocorticoid negative feedback inhibition under normal, non-stress conditions, (3) histaminergic neurons stimulate the HPA axis but may not be able to maintain their activity for extended periods of time, and (4) glucocorticoid negative feedback inhibition can occur but may only be effective within a specific period after HPA activation due to stress.
7
Zollner, Ekkehard Werner Arthur. "Hypothalamic-pituitary-adrenal axis suppression in asthmatic children on corticosteroids." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/95468.
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Thesis (PhD)-- Stellenbosch University, 2013.<br>ENGLISH ABSTRACT: Although the effect of inhaled corticosteroids (ICS) on the hypothalamic- pituitary-adrenal
axis (HPA) has been regarded as a “benign physiological response”, a survey published in
2002 suggested that adrenal crisis is more common in asthmatic children on ICS than
previously thought. Relying on clinical features to detect chronic adrenal insufficiency
secondary to corticosteroids may not be wise, as these are non-specific and can therefore
easily be missed. Accurate biochemical assessment of the whole axis to detect subclinical
HPA suppression (HPAS) is thus desirable. A review of the literature indicates that basal
adrenal function tests, including plasma cortisol profiles, do not identify which children can
appropriately respond to stress. There is no evidence to suggest that the degree of the
physiological adjustment of the HPA to ICS and/or nasal steroids (by reducing basal cortisol
production), predicts HPAS. Cortisol profiles should therefore only be used to demonstrate
differences in systemic activity of various ICS and delivery devices. Only two tests,
considered as gold standard adrenal function tests [the insulin tolerance test (ITT) and the
metyrapone test] can assess the integrity of the whole axis.<br>AFRIKAANSE OPSOMMING: Die outeurs van ´n opname wat in 2002 gepubliseer is stel voor dat ´n bynierkrisis meer
algemeen by asmatiese kinders, wat inhalasie kortikosteroïede ontvang, voorkom as wat
voorheen gedink is. Dit is strydig met die gevestigde opvatting dat die effek van IKS op die
hipotalamiese-hipofise-bynier-as (HHB) ’n “goedaardige fisiologiese reaksie” is. Die kliniese
kenmerke van kroniese bynierontoereikendheid sekondêr tot die gebruik van kortikosteroïede
(KS) is nie-spesifiek en gevolglik onbetroubaar. ´n Akkurate biochemiese toets van
subkliniese HBB onderdrukking (HHBO) sou gevolglik waardevol wees. ´n Literatuur oorsig
toon dat toetse van basale bynierfunksie, insluitend plasma kortisol (K) profiele, nie kinders
uitken wat toepaslik op stres sal reageer nie. Daar is geen bewyse dat die graad van
fisiologiese aanpassing van die HHB, soos aangedui deur laer K-vlakke, na die gebruik van
IKS en/of nasale steroïede (NS), HHBO voorspel nie. Serum K profiele is dus slegs van
waarde om die sistemiese aktiwiteit van verskillende IKS en toedieningsstelsels te ondersoek.
Slegs twee toetse, naamlik die insulien toleransie toets (ITT) en die metyrapone -(MTP)-toets
(wat beide as die goue standaard van bynier funksie beskou word), kan die integriteit van die
hele as meet.<br>Stellenbosch University<br>Medical Research Council<br>SA Thoracic Society<br>Harry Crossley Foundation<br>Red Cross Children’s Hospital.
8
Kalyani, Manu. "Interaction between Prolactin and the Hypothalamic-Pituitary-Adrenal (HPA) axis." Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1397233916.
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9
Reynolds, Rebecca M. "Programming of the hypothalamic-pituitary-adrenal axis during fetal life." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23168.
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The aim of this thesis was to study the HPA axis in detail, examining aspects of both activity of the axis and cortisol action, in order to determine variations that could explain the link between low birthweight and subsequent development of cardiovascular risk factors. The principal findings were that men aged 66-77 years, who were of low birthweight and/or with the Metabolic Syndrome, have activation of the HPA axis with increased cortisol response to ACTH<sub>1-24</sub> and increased urinary cortisol metabolite excretion. In contrast to rats programmed by dexamethasone administration during pregnancy, there was no evidence of altered central feedback sensitivity to low dose dexamethasone. However, dexamethasone may not cross the blood-brain barrier at low doses in man, so that this only tests the pituitary component of the negative feedback loop. Alternatively, rather than impaired central negative feedback, the activation of the HPA axis could be due to increased forward drive to ACTH and cortisol secretion from higher centres. Consistent with this hypothesis there was lack of habituation to the stress of repeated venepuncture in diabetic subjects. In contrast to the central GR changes, peripheral (liver) GR expression is increased in the rodent model. Tissue-specific differences in GR levels are a potential mechanism whereby subtle abnormalities in cortisol action could contribute to variations in insulin sensitivity in the population. Using competitive quantitative RT-PCR, GR mRNA levels were determined in total RNA extracted from skeletal muscle biopsies from 23 men in Uppsala, Sweden who had been studied at age 70 years with an oral glucose tolerance test and a euglycaemic hyperinsulinaemic clamp. Increased GR expression was associated with resistance to insulin-mediated glucose uptake, independent of obesity.
10
Heinzmann, Jan-Michael. "Central and peripheral aspects of hypothalamic-pituitary-adrenal (HPA) axis dysfunction." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-150032.
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11
Sudlow, Allan William. "Actions of lipocortin-1 on the immune-hypothalamic-pituitary-adrenal axis." Thesis, University of Manchester, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618752.
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It is thought that the involvement of common mediators such as corticotrophin releasing hormone (CRR), cytokines, prostaglandins (PG's), pituitary peptides and glucocorticoids allows the integration of immune and neuroendocrine activity during the acute phase response (APR) to injury and infection. Glucocorticoids are the major inhibitory component within this complex system, which has been termed the immunehypothalamic- pituitary-adrenal (HPA) axis. In the past, lipocortin-1 (LC-1) has been implicated as a "second messenger" of glucocorticoid actions. The present study explored this potential role for LC-l in relation to the immune-HPA axis.
12
Connan, Frances. "An investigation of hypothalamic pituitary adrenal axis hyperactivity in anorexia nervosa." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419238.
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13
Hesketh, Shirley Anne. "Pharmacological manipulation of central serotonin and the hypothalamic-pituitary-adrenal axis." Thesis, University of Bristol, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404294.
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Porter, Richard J. "Corticosteroid serotonin interactions in depression." Thesis, University of Newcastle upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289200.
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15
Buss, Nicholas Alexander Piers Sascha. "The role of formyl peptide receptors within the hypothalamic pituitary adrenal axis." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/5849.
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Annexin 1 (ANXA1) is an important mediator of the regulatory effects of glucocorticoids (GCs) within the neuroendocrine and host defence systems. Recent data suggest that it acts via a formyl peptide receptor (FPR) as a mediator of the negative feedback effects of GCs on adrenocorticotrophic hormone (ACTH) release. In the present study, in vitro and in vivo methods were used to detect and explore further the function of these receptors within the hypothalamo-pituitary-adrenocortical (HPA) axis. Lipopolysaccharide (LPS), given intra-peritoneally (i.p.) or centrally (i.c.v.), increased expression of mRNAs for ANXA1 and Fpr1, Fpr2 and Fpr3 in the spleen, pituitary and adrenal gland, but not in the brain. Given i.p., it also caused inflammatory cell infiltration in the adrenal gland, but not the pituitary, together with decreased vacuolation in the steroidogenic cells, increases in serum pro-inflammatory cytokines and corticosterone (CORT) and a subsequent loss of sensitivity to ACTH. The increases in ANXA1, Fpr1 and Fpr3 expression were dependent on inflammatory cell infiltration (predominantly eosinophils) but those of Fpr2 were not. The decrease in vacuolation was also independent of the inflammatory cell infiltration but was severely compromised by deletion of the genes encoding ANXA1 and Fpr2. Pharmacological studies on isolated adrenal cells in vitro suggest that ANXA1 may act via Fpr2 to inhibit ACTH-stimulated CORT release but that Fpr1 effects a tonic stimulatory effect on ACTH-driven steroidogenesis. These data suggest that ANXA1 and the FPRs play an important role within the adrenal in mediating the HPA responses to endotoxin and provide new evidence to suggest that infiltrating leukocytes are are also important in this regard.
16
Symonds, Catherine. "The hypothalamic-pituitary-adrenal axis in depression : a focus on the hippocampus." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/the-hypothalamic--pituitary--adrenal-axis-in-depression-a-focus-on-the-hippocampus(65f9eca0-f831-4bf0-a934-0f3d21b8856c).html.
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Background: The hypothalamic-pituitary-adrenal (HPA) axis has been implicated in the aetiopathology of depression, and the incidence of HPA dysfunction tends to increase with the severity of treatment resistance. In healthy volunteers (HV), both acute and chronic hypercortisolaemia causes cognitive impairment, including emotional memory. The exact mechanism of this remains unclear; however the action of cortisol on corticosteroid receptors in the hippocampus appears to be crucial and this may also be important in the aetiopathology of depression. The aim of this thesis was to investigate acute and chronic states of the HPA axis, and its role on neurocognition in HV and treatment resistant depression (TRD). Methods: The acute action of cortisol in HV was examined through meta-analysis of the literature. In HV, the acute, non-genomic effects of hydrocortisone on the hippocampus were measured using pharmacological challenge functional magnetic resonance imaging (phMRI) and the effects on the working memory n-back task during functional magnetic resonance imaging (fMRI). Additionally, the neurocognitive effects in TRD patients, who are theorised to have chronically elevated corticosteroids, were compared to age and sex matched HV using the n-back task and a novel emotional encoding-retrieval task. Finally the acute effects of hydrocortisone on the whole brain were measured in TRD compared to HV using phMRI.Results: Meta-analysis results demonstrated an adverse effect on performance in retrieval tasks, but not encoding, after an acute rise in cortisol in HV, with a trend towards sparing of emotional memories. Using phMRI, hydrocortisone caused a time dependent increase in signal in the hippocampus, as well as an increased signal in the ventrolateral prefrontal cortex and a decreased signal in the hippocampus during the n-back task. Patients with TRD, when compared with HV, had a decreased signal in the dorsolateral prefrontal cortex during the n-back task. Additionally, during the emotional encoding-retrieval task, regardless of the emotional content, the patients showed a decrease in signal in the posterior cingulate during encoding and an increase in the posterior insula during retrieval. During retrieval of positive versus neutral images, there was an increase in signal in the anterior cingulate. The earlier phMRI findings were not reproduced in either the TRD or age and sex matched controls. Conclusions: This work developed and examined a new technique to explore the relationship between the HPA axis and depression, as well as exploring the neurocognitive difference between TRD and HV. A non-genomic, acute effect of cortisol on the hippocampus was demonstrated in HV, as well as differences in processing emotional memories both acutely in HV and also in TRD patients. Further work needs to be done to develop the phMRI technique further and explore the aetiopathological role of the HPA axis in depression, focussing on the hippocampus.
17
Bakirtzi, Georgia. "Epigenetic regulation of POMC : implications for the hypothalamic-pituitary-adrenal (HPA) axis." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9455/.
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Crane, James William. "Limbic system control of endocrine stress responses /." St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16769.pdf.
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Beck, Meredith Nell. "Effects of Prolactin on the Hypothalamic Pituitary Adrenal Axis in Postpartum Female Rats." Miami University Honors Theses / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1303497697.
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Nye, Elisabeth Jane. "Dynamic stimulation tests in the assessment of hypothalamic-pituitary-adrenal axis function in pituitary disease and obesity /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17166.pdf.
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21
Janse, van Vuuren Marthinus. "Hypothalamic-pituitary-adrenal-axis vs. the sympatho-adrenal medullary system in the acute response to psychological stress." Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/6738.
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Thesis (MSc (Physiological Sciences))--University of Stellenbosch, 2011.<br>Includes bibliography.<br>ENGLISH ABSTRACT: The hypothalamic-pituitary-adrenal-(HPA) axis has long been closely associated with
psychological stress-induced activation of the adrenal cortex and subsequent glucocorticoid
production. Another, less known peripheral limb of the psychological stress response, is the
sympatho adrenal medullary pathway.
We hypothesized that the sympatho-adrenal medullary system constitutes the primary response
to acute psychological stress, with the HPA-axis functioning as a secondary response. We tested
our hypothesis by manipulating a model of acute mild psychological stress (restraint) by
blocking IL-6, a valuable constituent of the sympatho-adrenal medullary system.
Serum corticosterone concentration increased in response to stress (7 ± 3 vs. 57 ± 4 ng/ml;
P<0.0001), a response attenuated when IL-6 was blocked (17 ± 7 ng/ml). Stress increased
pituitary mass only when IL-6 was blocked (38 ± 3 vs. 65 ± 6 mg; P <0.001). Stress increased
left adrenal mass only in the presence of IL-6 (34 ± 1 vs. 73 ± 8 mg; P <0.00001). Stress did not
influence the circulating levels of TNF-α, IL-1β or IL-6 significantly. IL-1β and TNF-α
concentrations in the unstressed rats were lower when IL-6 was blocked.
We then manipulated the stress model by administering S. frutescens extract to elucidate both the
central and peripheral effects of acute S. frutescens administration on the psychological stress
response.
Restraint caused decreases in hippocampal GR levels when compared to respective controls. S.
frutescens administration and exposure to restraint synergistically decreased hippocampal
GABAAR levels. In addition, exposure to both stress and S. frutescens led to a noteworthy
increase in pituitary mass (P = 0.078), as well as pituitary ACTH levels (P < 0.01). Similarly,
differences in circulating ACTH levels showed an effect of stress on ACTH secretion only in the
presence S. frutescens (P < 0.05). Adrenal mass was significantly increased in S. frutescenstreated
animals that were also exposed to restraint (P < 0.05). Adrenal levels of ACTH showed a
reciprocal trend to pituitary and circulating ACTH levels. No statistically significant differences
were seen in adrenal IL-6 content. However, marked increases in IL-6 levels were seen at this
level with administration of S. frutescens stress exposure and a cumulative increase seen with
both S. frutescens-treatment and stress exposure.
Hippocampal GABAAR, pituitary mass, pituitary ACTH and circulating ACTH levels showed a
similar trend towards a synergistic effect of S. frutescens and restraint in activation of the
psychological stress response, while adrenal ACTH levels showed an inverse trend.
Hippocampal GR did not show any effect of stress or S. frutescens-treatment.
The results from these two experiments indicate that the sympatho-adrenal medullary system
constitutes the primary response to acute mild psychological stress and that the HPA-axis is only
activated during an exacerbated stress response or when the sympatho-adrenal medullary
contribution is inadequate. Furthermore, the acute administration of S. frutescens possibly led to
a functional shift in GABAergic function, resulting in activation of the stress response. The
anecdotal reports of a “docile” effect of S. frutescens most likely results from activation of the
mesolimbic dopaminergic system by the hippocampus and amygdala. These results have
dramatic consequence in GABA-based anxiety-treatments.<br>AFRIKAANSE OPSOMMING: Die hipotalamo-pituïtêre-adrenale (HPA)-as is lank bekend as ‘n primêre rolspeler in die respons
op emosionele stres en daaropvolgende glukokortikoïed produksie. ‘n Ander, minder bekende
arm van die sielkundige stres respons is die simpatiese bynier-medulla-sisteem.
Ons hipotese was dat die laasgenoemde simpatiese bynier-medulla-sisteem die primêre respons
tot sielkundige stres behartig terwyl die HPA-as ‘n sekondêre respons bied. Ons het ons hipotese
getoets deur die manupilering van ‘n beproefde stres model waar ons IL-6, ‘n waardevolle
rolspeler in die simpatiese bynier-medulla-sisteem, onderdruk het.
In respons op stress, het serum kortikosteroon konsentrasies toegeneem slegs in die
teenwoordigheid van IL-6 (7 ± 3 vs. 57 ± 4 ng/ml; P<0.0001), maar nie wanneer IL-6 onderdruk
is nie (17 ± 7 ng/ml). Stres het ‘n verhoging in hipofise massa teweeggebring slegs tydens die
onderdrukking van IL-6 (38 ± 3 vs. 65 ± 6 mg; P <0.001). Stres het ook linker-byniermassa
verhoog slegs wanneer voldoende IL-6 beskikbaar was (34 ± 1 vs. 73 ± 8 mg; P <0.00001).
Stres alleen het geen invloed gehad op serum IL-1β, IL-6 of TNF-α nie, maar die onderdrukking
van IL-6 het wel ‘n inhiberende effek op basale IL-1β en TNF-α gehad.
Daarna het ons weer eens die stresmodel manipuleer deur die rotte ‘n S. frutescens ekstrak te gee
in ‘n poging om beide die sentrale en perifere effekte daarvan op die sielkundige stres respons te
evalueer.
Stres alleen het gelei tot ‘n afname in GR terwyl ‘n kombinasie van stres en S. frutescens
administrasie tot ‘n afname in GABAARα1 in die hippokampus gelei het. Hierdie kombinasie
het ook tot ‘n merkwaardige toename in hipofise massa (P = 0.078) sowel as ACTH-inhoud van
die hipofise (P < 0.01) gelei. ‘n Soortgelyke patroon is waargeneem betreffende sirkulerende
ACTH en byniermassa met P < 0.05 vir elk. Bynier ACTH inhoud, aan die ander kant, het ‘n
omgekeerd eweredige verhouding met ACTH in die hipofise en in sirkulasie getoon. Bynier IL-
6 inhoud het geen statisties beduidende verskille getoon nie, maar ‘n merkwaardige verhoging is
weereens gesien met ‘n kombinasie van stres en S. frutescens administrasie.
Die soortgelyke tendens wat waargeneem word in GABAAR in die hippokampus, asook
hipofise- en sirkulerende ACTH vlakke, en dui op ‘n samewerkende rol van stres en S. frutescens
in die aktivering van die sielkundige stres respons. GR in die hippokampus toon geen
veranderinge nie. Die resultate van die twee eksperimente dui op ‘n primêre rol van die
simpatiese bynier-medulla-sisteem in die respons op ‘n akute stressor en dat die HPA-as net
geaktiveer word tydens ‘n ooreiste stres reaksie of indien die simpatiese bynier-medulla-sisteem
onderdruk word. Die waargenome “verdowings”-effek van S. frutescens word moontlik deur
aktivering van die mesolimbiese dopamien pad deur die hippokampus en amigdala bewerkstellig.
Die resultate mag ook lei tot die heroorweging van GABA-gebaseerde angs medikasies.
22
Dumbell, Rebecca. "The role of the hypothalamic-pituitary-growth axis in the regulation of seasonal and exercise induced weight gain in the Siberian hamster." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid+214824.
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The Siberian hamster (Phodopus sungorus) undergoes a suite of physiological changes in response to short day (SD) photoperiod which includes a marked reduction in body mass (up to 40%). This altered physiology can be reversed by a return to long day (LD) photoperiod and is driven by changes hypothalamic gene expression. Additionally, stimulation of weight regain occurs through spontaneous exercise when hamsters are provided with a running wheel (RW), despite intact photoperiod appropriate hypothalamic gene expression. The foundation hypothesis for this investigation was that the change in body weight in both paradigms is underpinned by an alteration of the growth hormone (GH) axis. Pasireotide, a somatostatin agonist, was utilised to inhibit GH secretion from the pituitary in both paradigms. Measurement of body mass, mass of internal organs, body composition by magnetic resonance imaging, hormonal analysis and in situ hybridization were used to determine the effect of a blockade of GH secretion by pasireotide. Pasireotide suppressed the GH axis in Siberian hamsters; with reduced circulating insulin-like growth factor-1 and altered hypothalamic gene expression of somatostatin (srif) and growth hormone – releasing hormone (ghrh) consistent with an inhibition of pituitary GH secretion. Pasireotide treatment inhibited RW and LD stimulated growth, and when administered to LD hamsters caused weight loss in a similar manner to that which occurs in SD and accompanied by testicular atrophy. In addition, pasireotide increased the incidence of torpor and increased bout length of this hypometabolic state in sedentary SD hamsters. In conclusion, evidence is provided for the hypothalamic – pituitary – growth hormone axis in the determination of photoperiod and RW induced body weight changes. Furthermore, the data show evidence for a novel muscle – brain pathway and evidence for a neuroendocrine pathway involved in torpor induction.
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Bruner, Natalie R. "Effects of prenatal stress on lever-press acquisition, delay discounting, and ethanol self-administration in rats." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/10882.
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Thesis (Ph. D.)--West Virginia University, 2010.<br>Title from document title page. Document formatted into pages; contains vi, 67 p. : ill. Includes abstract. Includes bibliographical references (p. 59-67).
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Jeffray, Treena. "The effects of cortisol on the development of the fetal hypothalamic-pituitary-adrenal axis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ41180.pdf.
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Tannenbaum, Beth. "Hypothalamic-pituitary-adrenal axis regulation over the lifespan : contribution of dietary and lifestyle factors." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36842.
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A delicate balance exists between the protective effects of adrenal glucocorticoids (GCs) secreted in response to stress and the negative consequences that the excessive production of these hormones may have for numerous systems. GCs are involved in the regulation of the stress response, have effects on feeding and body weight gain and are associated with the acceleration of central nervous system aging. Their production, secretion, and containment are subject to both environmental modulation and individual variation. Neonatal manipulations known to affect the development of the adult hypothalamic-pituitary-adrenal (HPA) response to stress had profound effects on both basal and stress-induced dietary choice, body weight and insulin dynamics. We followed this study with an examination of how the physiological and emotional response to stress can affect diet choices and affective status. Stress had an impact on diet choice and had a strong effect on emotional status but did not affect subjects uniformly. We then explored the reciprocal relationship, i.e. how diet itself can affect the response to stress and found that basal and stress-induced activation of the HPA axis in both young and aged rats is augmented following the feeding of high-fat diets and fat-feeding cause aberrations in glucose-insulin axis. Since aging can be associated with profound changes in HPA axis function, we assessed how dietary habits may contribute to the emergence of the cortisol (F) profile in a population of healthy elderly humans. We found a strong positive relationship between individual F production, feelings of depression and the high fat content in their diets. While dietary habits may have a negative impact on the emergence of an individuals' cortisol profile and on the aging process, we wanted to explore whether a beneficial intervention at mid-life would allow animals to age "successfully" by reducing glucocorticoid production. Environmental enrichment lowered corticosterone lev
26
Hawkins, Paul. "Nutritional influences on development of the cardiovascular system and the hypothalamic-pituitary-adrenal axis." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325124.
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Faghih, Rose Taj. "The FitzHugh-Nagumo model dynamics with an application to the hypothalamic pituitary adrenal axis." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/60161.
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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2010.<br>Includes bibliographical references (p. 68-70).<br>In this thesis, I revisit the issue of the utility of the FitzHugh-Nagumo (FHN) model for capturing neuron firing behaviors. It has been noted (e.g., see [8]) that the FHN model cannot exhibit certain interesting firing behaviors such as bursting. I will illustrate that, by allowing time-varying parameters for the FHN model, one could overcome such limitations while still retaining the low order complexity of the FHN model. I also highlight the utility of the FHN model from an estimation perspective by presenting a novel parameter estimation method that exploits the multiple time scale feature of the FHN model, and compare the performance of this method with the Extended Kalman Filter through illustrative examples. Then, I apply this proposed extension to the FHN model to model cortisol secretion, which is controlled by the hypothalamic pituitary adrenal axis (HPA). Existing mathematical models for cortisol secretion do not include the entire cortisol secretion process, from the neural firing of cortopin releasing hormone(CRH) in the hypothalamus to cortisol secretion in a deterministic manner. I lay the groundwork to construct a more comprehensive model, relating CRH, Adrenocorticotropic hormone (ACTH), and cortisol. I start with one of the existing cortisol mathematical models, and add to it a simplified neural firing model to describe the CRH and ACTH release. This simplified neural firing model is obtained using the FHN model with time-varying spiking threshold. Moreover, I include a feedback in this model and model the cortisol secretion as a tracking problem.<br>by Rose Taj Faghih.<br>S.M.
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Cullen, Alexis Elizabeth. "Increased stress susceptibility and hypothalamic-pituitary-adrenal axis dysfunction : early markers of psychosis vulnerability?" Thesis, King's College London (University of London), 2014. http://kclpure.kcl.ac.uk/portal/en/theses/increased-stress-susceptibility-and-hypothalamicpituitaryadrenal-axis-dysfunction(b602f1f0-1006-4491-a112-83d5156f8e13).html.
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Background: Individuals with psychosis are characterised by increased exposure and reactivity to psychosocial stressors and abnormal hypothalamic-pituitary-adrenal (HPA) axis function [i.e., elevated cortisol levels, a blunted cortisol awakening response (CAR), and pituitary volume abnormalities]. The extent to which these features are present among at-risk individuals, prior to illness onset, is currently unclear. Aims: To determine whether putatively at-risk children who present multiple antecedents of schizophrenia (ASz) or a family history of illness (FHx) show increased susceptibility to psychosocial stressors and HPA axis abnormalities relative to typically-developing (TD) children. An additional aim was to explore associations between these measures and neurocognitive function. Methods: ASz (n=35), FHx (n=25), and TD (n=44) children were identified at age 9-12 years using a novel community-screening procedure or as relatives of individuals with schizophrenia. Measures of psychosocial stress, salivary cortisol, pituitary volume, and neurocognitive function were obtained at age 11-14 years. Results: Relative to TD children, both ASz and FHx children reported greater exposure to psychosocial stressors and were more distressed by these exposures (d=0.55-1.02, p<0.05). Additionally, FHx children, but not ASz children, showed a blunted CAR compared to TD children (d=0.73, p=0.01), yet neither group were characterised by elevated diurnal cortisol levels or pituitary volume abnormalities. In exploratory analyses, more abnormal HPA axis function (i.e., higher diurnal cortisol levels and a more blunted CAR) was associated with greater neurocognitive deficits among FHx and ASz children, whilst experiences of psychosocial stress were associated with better neurocognitive performance.
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Steele, Amber. "Cortisol and mood as a function of luteal progesterone change : a prospective cohort study in Cambridge using diary methods and biological samples." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610359.
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Dettmer, Amanda M. "Early rearing experience, hypothalamic-pituitary-adrenal (HPA) activity, and serotonin transporter genotype influences on the development of anxiety in infant rhesus monkeys (Macaca mulatta) /." Amherst, Mass. : University of Massachusetts Amherst, 2009. http://scholarworks.umass.edu/open_access_dissertations/45/.
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Williamson, Martin Alexander. "Unmasking the functional anatomy of medial preoptic nucleus-influences on the hypothalamic-pituitary-adrenal axis." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/7628.
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The hypothalamic-pituitary-adrenal (HPA) axis is a critical mediator of the stress response
system. However, despite clear evidence for an inhibitory role of testosterone on stress-induced
activation of the HPA axis, the routes and mechanisms have not been addressed. To first
determine where testosterone acts in the brain to regulate stress-related input to the HPA axis, I
used a combined retrograde transport and immunohistochemical procedure to characterize the
anatomical nature by which androgen targets in the brain communicate with the paraventricular
nucleus (PVN) of the hypothalamus, the initial point of the neuronally mediated stress response.
The findings suggest that androgens could act throughout the brain, and on a large assortment of
brain regions that innervate the PVN. Among the brain regions identified, neurons of the medial
preoptic nucleus (MPN), highly express androgen receptors and project abundantly to the PVN,
suggesting that the MPN stands out as a potential site of integration between testosterone and the
HPA axis. To test the functional role of these cells, I tested whether lesions of the MPN alter the
inhibitory effects of testosterone on the HPA axis. By selectively removing cells in the MPN,
testosterone regulation of the PVN and HPA axis was eliminated. Together, these findings
demonstrated that the integrity of the MPN is essential in maintaining the regulatory effects of
testosterone on the brain's response to stress. Finally, to clarify whether the MPN is the seat of,
or an obligatory relay for the central effects of testosterone, I tested the effects of implanting the
androgen receptor antagonist hydroxyflutamide into the MPN, on the stress-induced activation of
the PVN and HPA output. The differential effects of androgen exposure in the MPN on the
biosynthetic capacity and activational responses of the PVN and its extended circuitries
suggested that the MPN is capable of bridging converging limbic influences to the HPA axis
with changes in gonadal status.<br>Medicine, Faculty of<br>Graduate
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Dembek, Katarzyna Agnieszka. "Renin-Angiotensin-Aldosterone System (RAAS) and Hypothalamic-Pituitary-Adrenal Axis (HPAA) in Critically Ill Foals." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337797078.
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Pyter, Leah M. "Seasonal plasticity of physiological systems, brain, and behavior." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141319505.
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Bingham, Brenda. "Role of neonatal testosterone in shaping the adult male hypothalamic-pituitary-adrenal axis response to stress." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/40838.
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Testosterone exposure during critical periods of development exerts major organizing effects on the hypothalamic-pituitary-adrenal (HPA) axis. The aim of this thesis was to determine how HPA axis activity is altered by neonatal testosterone, and where and how this might occur in the adult brain. In chapter two, I demonstrate that neonatal gonadectomy increased plasma corticosterone and Fos activation in the ACTH-regulating zone of the paraventricular nucleus of the hypothalamus under basal conditions and following restraint exposure. These responses were normalized with postnatal, but not adult testosterone replacement. Neonatal gonadectomized rats also had decreased numbers of AR and arginine vasopressin-positive cells in the bed nucleus of the stria terminalis and medial amygdala. This suggests that testosterone exposure during the neonatal period may prime adult HPA response to testosterone by altering AR levels and function within afferent mediators of HPA axis activity. Testosterone in the brain can be converted to estradiol by the aromatase enzyme, and estradiol usually impacts brain development directly. In chapter 3, I demonstrate that animals neonatally exposed to aromatase, or AR blockade fail to show a normal decline in corticosterone, or habituate, in response to repeat restraint exposure. By contrast, males castrated as adults show a significant reduction in corticosterone after repeated stress. These findings suggest an organizing influence of both ARs and estrogen conversion on HPA habituation, which occurs independently of activational effects of testosterone. The immediate early gene c-fos is rapidly induced in many brain regions following acute restraint stress and is an excellent tool for mapping functional differences in brain activation by stress. In chapter 4, we used c-fos mRNA as a tool to map changes in cellular activation in acutely stressed adult animals that received aromatase blockade neonatally. This treatment enhanced stress-induced c-fos expression in several limbic regions, including within the anterior cingulate and medial prefrontal cortex, lateral septum, anterior hypothalamic area, dorsal medial hypothalamus and medial amygdala, as well as at multiple levels of somatosensation. Based on these results, I propose estrogens exert effects during the neonatal period that result in systems-wide differences in adult neuroendocrine responses to homeostatic threat.
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Schmidt, Kristin. "Manipulating the hypothalamic-pituitary-adrenal axis : effects on cognitive and emotional information processing and neural connectivity." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:c0475a98-e070-4446-9179-eb87047cb854.
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Despite extensive evidence documenting abnormal hypothalamic-pituitary-adrenal (HPA) axis functioning as a risk factor for the development of depression and other psychiatric disorders, and experimental evidence from acute stress manipulations, the effects of sustained cortisol alterations on clinically relevant cognitive-behavioural and neural processing remain poorly understood. The aim of this thesis was to characterise how non-acute changes in cortisol levels modify behavioural and neural biases implicated in stress-related disorders by following two complementary lines of evidence: firstly, by increasing cortisol via a direct pharmacological intervention; and secondly, by testing the ability of gut microbiota manipulations to alter cortisol reactivity. The first study found that sustained increases in cortisol following 10-day administration of hydrocortisone were associated with altered memory and emotional processing in healthy volunteers. Specifically, participants receiving hydrocortisone showed enhanced recognition of emotional words, while their neutral memory performance was unaffected despite lower parahippocampal and occipital activation during viewing and encoding of neutral pictures. Furthermore, we found that resting-state functional connectivity between limbic-temporal regions of interest (amygdala and hippocampus) and the striatum (head of the caudate), as well as frontal and prelimbic cortices was decreased. In contrast, hippocampal and visual processing during negative facial expressions, and functional connectivity between the amygdala and the brainstem at rest, were increased in the hydrocortisone versus placebo groups. Overall, these findings suggest that non-acute increases in glucocorticoids enhance processing of emotionally salient information in limbic-temporal regions, which may modulate further neural mechanisms of sensory and homeostatic relevance. Enhancements in declarative emotional memory following hydrocortisone also implicate the modulation of amygdalar-hippocampal interactions by cortisol. Conversely, neutral stimulus processing was found to be either reduced or unaffected across a number of cognitive and memory domains. A specific increase for negative processing was further supported by poorer self-reported well-being at the mid-point of the study in participants receiving hydrocortisone. In a separate study exploring the ability of prebiotic supplements to affect cortisol reactivity and emotional processing, a Bimuno-galactooligosaccharide prebiotic was found to reduce the waking cortisol response and increase positive versus negative attentional processing in healthy volunteers. While these effects were not found to be associated, they provide initial promising evidence of the ability to target the HPA axis and emotional processing via the gut microbiota in humans. Overall, this thesis supports the idea that stress-induced physiological changes after prolonged or repeated cortisol exposure are associated with neural and behavioural alterations, which in turn have been crucial in understanding neuropsychological mechanisms underlying psychiatric disease. A better stratification of the effects of sustained HPA axis alterations on psychiatrically relevant cognitive-emotional domains and neural mechanisms thus remains of high priority.
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Farag, Noha Hassan. "Effect of physical activity on hypothalamic-pituitary-adrenal axis functioning in a multiracial sample of adolescents." Oklahoma City : [s.n.], 2009.
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Barugh, Amanda Jayne. "Delirium and long-term cognitive impairment after stroke : the role of the hypothalamic-pituitary-adrenal axis." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28800.
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Delirium is a severe neuropsychiatric syndrome, characterised by the acute onset of inattention, altered level of arousal, and other mental status abnormalities. Delirium is extremely common in acute stroke, affecting at least 1 in 5 such patients admitted to hospital. It is a serious complication of stroke, being associated with higher mortality, longer length of hospital stay and higher dependency at discharge. The pathophysiology of delirium is not completely understood, and there are no specific treatments. This thesis investigated the role of cortisol in the development of delirium after stroke and also investigated the role of delirium and of cortisol in the development of cognitive impairment in the 12 months after stroke. The thesis specifically investigated whether levels of cortisol in saliva are elevated in delirium and also whether there is a loss of the normal diurnal rhythm in delirium, evidenced by elevated afternoon salivary cortisol levels and reduced morning level to afternoon level ratio. The thesis also investigated whether cortisol levels are persistently elevated in the year after stroke in those who developed delirium and whether cortisol levels are associated with cognitive decline. Finally it investigated whether acute and/or chronic changes seen on Computed Tomography (CT) brain scans taken around the time of stroke onset are associated with the development of delirium after stroke A longitudinal cohort study was conducted in 95 participants aged 60 years or over, who were admitted to hospital with a clinically confirmed stroke. Participants gave informed consent, or proxy consent was obtained if they lacked capacity to consent. At baseline participants underwent brief cognitive testing and were then assessed for the presence of delirium, using DSM IV criteria, at regular intervals during the first two weeks after stroke. At each assessment a saliva sample was collected in the morning and in the afternoon, to measure cortisol. Participants were then visited at 1 month, 4 months and 12 months after stroke onset, at which point they were assessed for the presence of delirium, further saliva samples were taken and a cognitive test battery was completed. 26 (27%) participants developed delirium during the course of the study period. The study found elevated salivary cortisol levels in those with delirium at up to 4 months after stroke, but at 12 months there was no difference between the delirium and no delirium group. A loss of the diurnal rhythm was seen in those who developed delirium at 5 days after stroke, but the diurnal variation had returned to a normal pattern at follow-up. However, in a multivariate analysis, controlling for age, sex, stroke severity (NIHSS), current illness burden (APACHE II), chronic illness burden (CCI) and prior cognitive impairment (IQCODE), neither median salivary cortisol levels in the first two weeks after stroke, nor the ratio of morning to afternoon cortisol levels were independent predictors of delirium diagnosis, although median 9am cortisol approached significance (OR=0.95, 95% confidence interval (CI) 0.89-1.01, p=0.08). In a random effects logistic regression analysis, the probability of developing delirium decreased over time from stroke onset and increased per unit increase in salivary cortisol (nmol/L), however this effect was not statistically significant (OR 1.02, CI 0.84-1.19 P=0.70 for morning cortisol and OR 1.05, CI 0.82-1.25 p=0.46 for afternoon cortisol). Global cognition, measured by the MoCA, was significantly poorer in the delirium group at each time point throughout the 12 months after stroke. However, there was a trend towards improvement in MoCA scores in the whole cohort throughout the 12 month follow-up, with the exception of those who developed the most severe delirium. The presence of delirium at any point during the 12 month follow-up did not affect the rate of change of the MoCA scores over the 12 months after stroke. The presence of brain atrophy identified on admission CT brain scans was independently associated with delirium (OR 3.7, CI 1.15-11.88, p=0.02), however the presence of a visible acute or chronic stroke lesion and the presence of white matter lesions were not. Finally, those who developed delirium had a worse functional outcome, longer length of hospital stay and were more likely to require institutional care or a package of care at home, compared with those who did not develop delirium. This thesis has contributed to our understanding of the mechanisms and phenomenology of delirium after stroke, and has also highlighted areas for further research which will be required to unpick the complex pathophysiology of delirium.
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Barnum, Christopher John. "Repeated exposure to restraint but not social defeat leads to habituation of the pituitary-adrenal and stress-herthermic responses." Diss., Online access via UMI:, 2006.
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Coleman, Georgia. "Effects of postnatal light environment on the development of the mouse stress system." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/effects-of-postnatal-light-environment-on-the-development-of-the-mouse-stress-system(1cb0bdca-3aaa-4d92-879c-98131575aff2).html.
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The postnatal period is a critical time for development where external influences can help shape the long-term structure and function of the brain. Adverse experiences or stressors during the postnatal period, such as abuse or neglect, can have huge consequences on the long term function, health and susceptibility to disease. One environmental factor, whose importance is becoming increasingly more recognised for normal development, is light. Abnormal light during the first three weeks of life has been shown to have long term effects on the circadian system of rodents. On the other hand, the effects of abnormal light during the postnatal period on the stress system have yet been relatively unexplored. Therefore the aim of this thesis was to assess if altered postnatal light environment, such as that a preterm baby might be exposed to, has any long-term effects on the stress system. Mice were raised under constant light (LL), constant darkness (DD) or a normal 12:12hr light:dark cycle (LD) for the first three weeks of life from postnatal day (P)1 up until P21. From P21, all mice were then housed in LD conditions and the stress system was assessed by looking at several different levels of the HPA axis including neuropeptide expression in the brain, body and adrenal weight, and plasma corticosterone levels under both basal and stressed conditions. Learning and memory, anxiety-like behaviour and circadian output rhythms were also evaluated. Finally, mother-pup behaviour and maternal HPA axis were assessed to see if maternal care was changed by altered postnatal light. Both LL and DD rearing caused changes in the HPA axis of offspring with LL raised mice showing alterations in neuropeptide and glucocorticoid receptor expression in the brain. Postnatal DD resulted in a blunted corticosterone response to a stressor in females but had no effect in males. In terms of behaviour, LL raised mice had increased depressive-like behaviour. In contrast, postnatal light appears to have no effect on learning and memory or anxiety behaviour. When we looked at circadian output rhythms, we found that LL rearing appears to confer resilience to the rhythm disrupting effects of LL later on in life as seen by the maintenance of locomotor activity, body temperature and plasma corticosterone rhythms in LL. Maternal care and maternal stress systems appeared unaltered under the different postnatal light environments suggesting that the changes we see in the offspring are attributed to mechanisms other than alterations in maternal care.
40
Daniel, Joseph A. "Comparison of caesarian section and vaginal birth in pigs /." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9962516.
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Edwards, Lisa J. "Maternal undernutrition and fetal blood pressure and the hypothalamo-pituitary adrenal axis in the late gestation fetal sheep." Title page, table of contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phe2654.pdf.
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Includes bibliographical references (leaves 228-257). Aims to determine the impact of maternal undernutrition during late gestation and during the periconceptional and gestational periods on fetal growth, fetal blood pressure and the fetal hypothalamo-pituitary adrenal axis in the sheep.
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Khalili-Mahani, Najmeh 1971. "Observing the stressed brain : magnetic resonance imaging of the neural correlates of hypothalamic pituitary adrenal axis function." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115857.
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The Hypothalamic Pituitary Adrenal (HPA) axis is the coordinator of adaptive responses to physical and psychological stress. The central nervous system plays a key role in modulation of both basal and adaptive HPA axis functions. In fact, since long ago, animal studies have shown that acute and chronic exposure to glucocorticoids (a stress hormone released due to HPA axis activation, cortisol in humans) affects the function and the morphology of brain areas such as the hippocampus and the cingulate cortex. This thesis is based on novel neuroimaging methodologies used to investigate the interactions of psychological stress, cortisol and the brain. It consists of three functional studies and a morphometric one. In the first functional study we show that the hippocampus (where glucocorticoid receptors are most abundant) plays a role in initiation of an HPA axis stress response. In the second study, we provide evidence that besides hippocampus, the neural activity in the so-called "default mode network" (DMN), especially the anterior cingulate cortex (ACC), relates to interindividual variations in HPA axis response to psychological stress. In the third study we have investigated the cortisol-modulation of the DMN. Again, we provide evidence for a role of the ACC and the orbitofrontal cortex in negative feedback inhibition of the HPA axis activity. Finally, we show a morphological link between the ACC and the cortisol response to awakening which is an index of basal HPA axis activity. Overall, our findings confirm the critical role of the ACC and mesolimbic system in HPA axis regulation. These findings also draw attention to the interactions between functional subregions of the medial prefrontal cortex and states of HPA axis function prior to stress onset---suggesting an interplay of the monitoring and the executive planning roles of the medial prefrontal cortex in behavioral adaptation to stress. Beyond stress research, our findings offer a framework for combining neuroimaging and neuroendocrinology to better understand the interindividual variances in behavior, and perhaps to better identify subgroups at risk of psychological disorders.
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Abebe, Getachew. "The integrity of the hypothalamic-pituitary-adrenal axis in Boran (Bos indicus) cattle infected with Trypanosoma congolense." Thesis, Brunel University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292991.
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Ward, Alexandra Monica Vivienne. "Fetal programming of the hypothalamic-pituitary-adrenal axis : is cortisol production upregulated centrally in low birthweight individuals?" Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400535.
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Grundy, Paul L. "The hypothalamic-pituitary-adrenal axis and hippocampal neutrophin responses to traumatic brain injury in relation to outcome." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399894.
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Osborne, Sarah Ann. "Antenatal depression and developmental programming of offspring hypothalamic-pituitary-adrenal axis in the first year of life." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/antenatal-depression-and-developmental-programming-of-offspring-hypothalamicpituitary(22ef00fa-ac36-48c6-a79f-0197ea03723d).html.
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Background: Research in humans demonstrates a link between an adverse environment during development and unfavourable health outcomes in adulthood. Animal research used to understand this phenomenon reveals that exposure to prenatal stress and to glucocorticoids may programme offspring hypothalamic-pituitary-adrenal (HPA) axis, which is in turn hypothesised to mediate disease risk. Extension of these findings in human research is at a less advanced stage, although synthesis of a number of lines of evidence suggests that similar HPA axis programming exists. Glucocorticoids are hypothesised as the final mediator in the pathway from adverse antenatal environment to programming effects, including altered offspring HPA axis activity, although molecular mechanisms underlying this hypothesis are yet to be elucidated. Depression in pregnancy is a paradigm by which mechanisms for developmental programming may be further studied. Methodology: A prospective longitudinal observational study of 82 pregnant women from the second trimester of pregnancy, and their offspring to 1 year postnatal is described. A cases group with DSM-IV major depressive disorder (MDD) was compared with a non-depressed control group. Maternal mood, antenatal HPA axis, obstetric outcomes and infant basal HPA axis activity and cortisol response to pain stress were assessed. Results: Compared with the control group, women with MDD in pregnancy had overactivity of the HPA axis in the third trimester of pregnancy, a shorter length of gestation, infants with larger cortisol response to pain stress at 8 weeks and 1 year postnatal and higher evening cortisol at 1 year of age. Furthermore, associations were found between antenatal depression, maternal antenatal HPA axis and infant HPA axis. The findings were independent of socio-demographic and obstetric factors and maternal postnatal mood. Conclusions: The associations between maternal antenatal depression and altered maternal and infant HPA axis activity suggest programming effects and add to the important literature on developmental programming in humans. Furthermore, the findings have clinical relevance in the fields of obstetrics, psychiatry and paediatrics.
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Warner, Judith Catherine. "Biology and Environment, Mothers and Infants: Linking Stress Physiology, Depression, Anxiety and Attachment." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/365334.
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The last two decades have seen research on early life experiences expand to include the prenatal environment and, more specifically, examination of the effects of prenatal maternal mental health on foetal and infant development. Cortisol, the hormonal end product of the Hypothalamic Pituitary Adrenal (HPA) Axis, has been identified as one mechanism associated independently with stress, pregnancy and mental health, which can account for changes during foetal development. In the postpartum, these early life experiences may serve as protective or risk factors for the infant. The longitudinal study conducted here examined nulliparous pregnant women (N = 40, Mage = 30.5, SD = 5.27) and their infants commencing during the first trimester of pregnancy until 12 months after birth, with the aim of identifying potentially modifiable mother-infant characteristics associated with mothers' mental health, infant stress physiology and attachment.
The longitudinal study was subdivided into four studies. First, in Study 1A, concurrent and prospective associations between maternal stress (cortisol and self-report of daily stress), coping, and mental health were examined across the three trimesters of pregnancy. Mothers completed questionnaires and gave saliva samples during each trimester of pregnancy and overall the findings showed the important role of coping in modulating baseline cortisol levels and anxiety in the face of daily stressors during pregnancy.<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy in Clinical Psychology (PhD ClinPsych)<br>School of Applied Psychology<br>Griffith Health<br>Full Text
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Spencer, Sarah J. "Stress and the brain : role of the medial prefrontal cortex in regulation of the hypothalamic-pituitary-adrenal axis /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18148.pdf.
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Larivière, William R. "The role of the hypothalamic-pituitary-adrenal axis in the susceptibility to adjuvant-induced polyarthritis in the rat." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ64597.pdf.
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Oates, Maxwell. "The role of leptin during neonatal rat development : impact on the hypothalamic-pituitary-adrenal axis and energy balance." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0032/MQ64419.pdf.
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