scholarly journals Effect of vasopressin 1b receptor blockade on the hypothalamic–pituitary–adrenal response of chronically stressed rats to a heterotypic stressor

2008 ◽  
Vol 200 (3) ◽  
pp. 285-291 ◽  
Author(s):  
Francesca Spiga ◽  
Louise R Harrison ◽  
Cliona P MacSweeney ◽  
Fiona J Thomson ◽  
Mark Craighead ◽  
...  
Keyword(s):  
White Noise ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Home Cage ◽  
Male Rats ◽  
Receptor Blockade ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosterone Secretion ◽  
Corticosterone Response ◽  
Adrenal Response

Exposure to chronic restraint (CR) modifies the hypothalamic–pituitary–adrenal (HPA) axis response to subsequent acute stressors with adaptation of the response to a homotypic and sensitization of the response to a heterotypic stressor. Since vasopressin (AVP) activity has been reported to change during chronic stress, we investigated whether this was an important factor in HPA facilitation. We therefore tested whether vasopressin 1b receptor (AVPR1B) blockade altered the ACTH and corticosterone response to heterotypic stressors following CR stress. Adult male rats were exposed to CR, single restraint, or were left undisturbed in the home cage. Twenty-four hours after the last restraint, rats were injected with either a AVPR1B antagonist (Org, 30 mg/kg, s.c.) or vehicle (5% mulgofen in saline, 0.2/kg, s.c.) and then exposed to either restraint, lipopolysaccharide (LPS) or white noise. CR resulted in the adaptation of the ACTH and corticosterone response to restraint and this effect was not prevented by pretreatment with Org. Although we found no effect of CR on LPS-induced ACTH and corticosterone secretion, both repeated and single episodes of restraint induced the sensitization of the ACTH, but not corticosterone response to acute noise. Pretreatment with Org reduced the exaggerated ACTH response to noise after both single and repeated exposure to restraint.

DEVELOPMENT OF HYPOTHALAMIC–PITUITARY–ADRENAL RESPONSE TO STRESS IN RATS MADE HYPOTHYROID BY EXPOSURE TO THIOURACIL FROM CONCEPTION

1981 ◽  
Vol 90 (3) ◽  
pp. 403-409 ◽  
Author(s):  
L. A. MESERVE ◽  
J. H. LEATHEM
Keyword(s):  
Hpa Axis ◽  
Adrenal Glands ◽  
Hypothalamic Pituitary Adrenal ◽  
Serum Corticosterone ◽  
Functional Maturation ◽  
State Delays ◽  
Corticosterone Secretion ◽  
Response To Stress ◽  
Adrenal Response

The functional maturation of the hypothalamic–pituitary–adrenal (HPA) axis has been studied in rats of 20–35 days of age made hypothyroid by the administration of thiouracil from conception. Basal concentrations of corticosterone in serum were normal in hypothyroid animals. Ether stress led to an increase in corticosterone content of the adrenal glands of hypothyroid and normal rats but not to a rise in serum corticosterone of hypothyroid rats until 30 days of age. Corticosterone secretion in response to ACTH administration was subnormal in hypothyroid rats. The hypothyroid state delays the development of the hypothalamic–pituitary–portion of the HPA axis until 30 days of age and causes a diminution in the adrenal response to ACTH beyond this time.

scholarly journals Hypothalamic-pituitary-adrenal axis up-regulation in rats submitted to pituitary stalk compression

2004 ◽  
Vol 180 (2) ◽  
pp. 297-302 ◽  
Author(s):  
PC Elias ◽  
LL Elias ◽  
M Castro ◽  
J Antunes-Rodrigues ◽  
AC Moreira
Keyword(s):  
Hpa Axis ◽  
Water Intake ◽  
Immobilization Stress ◽  
Male Rats ◽  
Pituitary Stalk ◽  
Salt Loading ◽  
Hypothalamic Pituitary Adrenal ◽  
Salt Load ◽  
Post Surgery

The present study investigated the hypothalamic-pituitary-adrenal (HPA) axis activity in response to stress in adult male rats submitted to pituitary stalk compression (PSC) or sham operation. Animals received water or oral salt loading (2% NaCl) for one or eight days before the day of the experiment. On the 14th day post-surgery rats were killed under basal conditions or after 15 min immobilization stress. In the PSC group urine output increased significantly and plasma vasopressin (AVP) levels failed to respond to osmotic stimuli. Short-term salt load induced a significant increase in AVP levels in the sham-operated group. The PSC group presented higher adrenocorticotrophin (ACTH) and corticosterone levels compared with sham-operated rats, both in water intake and salt load conditions. Immobilization stress induced a similar increase in plasma ACTH and corticosterone concentrations in sham-operated and PSC groups under water intake. However, long-term salt load blunted the ACTH and corticosterone responses to immobilization stress in sham-operated rats. PSC rats submitted to short- and long-term salt loading presented no changes in ACTH and corticosterone levels after immobilization. Immobilization stress caused neither AVP responses nor plasma osmolality changes in sham and PSC groups. There was no difference in median eminence AVP content among all groups. In conclusion, the high ACTH and corticosterone levels found in PSC rats under water intake and salt loading conditions suggest an up-regulation of the HPA axis, with a preserved adaptive mechanism to chronic stress.

scholarly journals Overexpression of Corticotropin Releasing Factor in the Central Nucleus of the Amygdala Advances Puberty and Disrupts Reproductive Cycles in Female Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (10) ◽  
pp. 3934-3944 ◽  
Author(s):  
X. F. Li ◽  
M. H. Hu ◽  
S. Y. Li ◽  
C. Geach ◽  
A. Hikima ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Pulse Generator ◽  
Female Rats ◽  
Central Nucleus ◽  
Ovariectomized Rats ◽  
Human Society ◽  
Central Administration ◽  
Corticosterone Secretion ◽  
Stress Changes

Abstract Prolonged exposure to environmental stress activates the hypothalamic-pituitary-adrenal (HPA) axis and generally disrupts the hypothalamic-pituitary-gonadal axis. Because CRF expression in the central nucleus of the amygdala (CeA) is a key modulator in adaptation to chronic stress, and central administration of CRF inhibits the hypothalamic GnRH pulse generator, we tested the hypothesis that overexpression of CRF in the CeA of female rats alters anxiety behavior, dysregulates the HPA axis response to stress, changes pubertal timing, and disrupts reproduction. We used a lentiviral vector to increase CRF expression site specifically in the CeA of preweaning (postnatal day 12) female rats. Overexpression of CRF in the CeA increased anxiety-like behavior in peripubertal rats shown by a reduction in time spent in the open arms of the elevated plus maze and a decrease in social interaction. Paradoxically, puberty onset was advanced but followed by irregular estrous cyclicity and an absence of spontaneous preovulatory LH surges associated with proestrous vaginal cytology in rats overexpressing CRF. Despite the absence of change in basal corticosterone secretion or induced by stress (lipopolysaccharide or restraint), overexpression of CRF in the CeA significantly decreased lipopolysaccharide, but not restraint, stress-induced suppression of pulsatile LH secretion in postpubertal ovariectomized rats, indicating a differential stress responsivity of the GnRH pulse generator to immunological stress and a potential adaptation of the HPA axis to chronic activation of amygdaloid CRF. These data suggest that the expression profile of this key limbic brain CRF system might contribute to the complex neural mechanisms underlying the increasing incidence of early onset of puberty on the one hand and infertility on the other attributed to chronic stress in modern human society.

scholarly journals Hypoactivity of the Hypothalamo-Pituitary-Adrenocortical Axis during Recovery from Chronic Variable Stress

Endocrinology ◽  
2006 ◽  
Vol 147 (4) ◽  
pp. 2008-2017 ◽  
Author(s):  
Michelle M. Ostrander ◽  
Yvonne M. Ulrich-Lai ◽  
Dennis C. Choi ◽  
Neil M. Richtand ◽  
James P. Herman
Keyword(s):  
Mrna Expression ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Male Rats ◽  
Plasma Acth ◽  
Novel Environment ◽  
Systemic Hypoxia ◽  
Delayed Recovery ◽  
Chronic Variable Stress

Chronic stress induces both functional and structural adaptations within the hypothalamo-pituitary-adrenocortical (HPA) axis, suggestive of long-term alterations in neuroendocrine reactivity to subsequent stressors. We hypothesized that prior chronic stress would produce persistent enhancement of HPA axis reactivity to novel stressors. Adult male rats were exposed to chronic variable stress (CVS) for 1 wk and allowed to recover. Plasma ACTH and corticosterone levels were measured in control or CVS rats exposed to novel psychogenic (novel environment or restraint) or systemic (hypoxia) stressors at 16 h, 4 d, 7 d, or 30 d after CVS cessation. Plasma ACTH and corticosterone responses to psychogenic stressors were attenuated at 4 d (novel environment and restraint) and 7 d (novel environment only) recovery from CVS, whereas hormonal responses to the systemic stressor were largely unaffected by CVS. CRH mRNA expression was up-regulated in the paraventricular nucleus of the hypothalamus (PVN) at 16 h after cessation of CVS, but no other alterations in PVN CRH or arginine vasopressin mRNA expression were observed. Thus, in contrast to our hypothesis, reductions of HPA axis sensitivity to psychogenic stressors manifested at delayed recovery time points after CVS. The capacity of the HPA axis to respond to a systemic stressor appeared largely intact during recovery from CVS. These data suggest that chronic stress selectively targets brain circuits responsible for integration of psychogenic stimuli, resulting in decreased HPA axis responsiveness, possibly mediated in part by transitory alterations in PVN CRH expression.

scholarly journals Facilitation of the HPA Axis to a Novel Acute Stress Following Chronic Stress Exposure Modulates Histone Acetylation and the ERK/MAPK Pathway in the Dentate Gyrus of Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 2942-2952 ◽  
Author(s):  
Chantelle L. Ferland ◽  
Erin P. Harris ◽  
Mai Lam ◽  
Laura A. Schrader
Keyword(s):  
Dentate Gyrus ◽  
Histone Acetylation ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Acute Stress ◽  
Male Rats ◽  
Stress Exposure ◽  
Erk Activation ◽  
Acute And Chronic Stress ◽  
Acute Stressor

Evidence suggests that when presented with novel acute stress, animals previously exposed to chronic homotypic or heterotypic stressors exhibit normal or enhanced hypothalamic-pituitary-adrenal (HPA) response compared with animals exposed solely to that acute stressor. The molecular mechanisms involved in this effect remain unknown. The extracellular signal-regulated kinase (ERK) is one of the key pathways regulated in the hippocampus in both acute and chronic stress. The aim of this study was to examine the interaction of prior chronic stress, using the chronic variable stress model (CVS), with exposure to a novel acute stressor (2,5-dihydro-2,4,5-trimethyl thiazoline; TMT) on ERK activation, expression of the downstream protein BCL-2, and the glucocorticoid receptor co-chaperone BAG-1 in control and chronically stressed male rats. TMT exposure after chronic stress resulted in a significant interaction of chronic and acute stress in all 3 hippocampus subregions on ERK activation and BCL-2 expression. Significantly, acute stress increased ERK activation, BCL-2 and BAG-1 protein expression in the dentate gyrus (DG) of CVS-treated rats compared with control, CVS-treated alone, and TMT-only animals. Furthermore, CVS significantly increased ERK activation in medial prefrontal cortex, but acute stress had no significant effect. Inhibition of corticosterone synthesis with metyrapone had no significant effect on ERK activation in the hippocampus; therefore, glucocorticoids alone do not mediate the molecular effects. Finally, because post-translational modifications of histones are believed to play an important role in the stress response, we examined changes in histone acetylation. We found that, in general, chronic stress decreased K12H4 acetylation, whereas acute stress increased acetylation. These results indicate a molecular mechanism by which chronic stress-induced HPA axis plasticity can lead to neurochemical alterations in the hippocampus that influence reactivity to subsequent stress exposure. This may represent an important site of dysfunction that contributes to stress-induced pathology such as depression, anxiety disorders, and posttraumatic stress disorder.

scholarly journals Hypothalamic-Pituitary-Adrenal Axis Activity of Newborn Mice Rapidly Desensitizes to Repeated Maternal Absence but Becomes Highly Responsive to Novelty

Endocrinology ◽  
2008 ◽  
Vol 149 (12) ◽  
pp. 6366-6377 ◽  
Author(s):  
L. Enthoven ◽  
M. S. Oitzl ◽  
N. Koning ◽  
M. van der Mark ◽  
E. R. de Kloet
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Hpa Axis ◽  
Mineralocorticoid Receptor ◽  
Maternal Separation ◽  
Mineralocorticoid Receptor Antagonist ◽  
Newborn Mice ◽  
Hypothalamic Pituitary Adrenal ◽  
The Third ◽  
Corticosterone Response

In CD1 mice we investigated the hypothalamic-pituitary-adrenal (HPA) axis response to maternal separation for 8 h daily from postnatal d 3 to 5. At d 3 a slow separation-induced corticosterone response developed that peaked after 8 h, and the pups became responsive to stressors. On the second and third day, the response to 8 h separation rapidly attenuated, whereas the response to novelty did not, a pattern reflected by the hypothalamic c-fos mRNA response. If maternal separation and exposure to novelty were combined, then after the third such daily exposure, the sensitivity to the stressor was further enhanced. Meanwhile, basal corticosterone and ACTH levels were persistently suppressed 16 h after pups were reunited with their mothers. To explain the HPA axis desensitization after repeated separation, we found that circulating ghrelin levels increased and glucose levels decreased after all periods of maternal separation, ruling out a role of altered metabolism. Glucocorticoid feedback was not involved either because a glucocorticoid receptor antagonist amplified the corticosterone response after the first but became ineffective after the third separation. In contrast, a mineralocorticoid receptor antagonist decreased and increased corticosterone levels after the first and third period of separation, respectively. In conclusion, the newborn’s HPA axis readily desensitizes to repeated daily maternal separation, but continues to respond to novelty in a manner influenced by a central mineralocorticoid receptor- rather than glucocorticoid receptor-mediated mechanism.

scholarly journals Inflammatory Pain and Corticosterone Response in Infant Rats: Effect of 5-HT1A Agonist Buspirone Prior to Gestational Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Irina P. Butkevich ◽  
Viktor A. Mikhailenko ◽  
Tat'yana R. Bagaeva ◽  
Elena A. Vershinina ◽  
Anna Maria Aloisi ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Inflammatory Pain ◽  
Formalin Test ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Plasma Corticosterone Level ◽  
Infant Rats ◽  
Corticosterone Response ◽  
Gestational Stress

Our researches have shown that gestational stress causes exacerbation of inflammatory pain in the offspring; the maternal 5-HT1A agonist buspirone before the stress prevents the adverse effect. The serotonergic system and hypothalamo-pituitary-adrenal (HPA) axis are closely interrelated. However, interrelations between inflammatory pain and the HPA axis during the hyporeactive period of the latter have not been studied. The present research demonstrates that formalin-induced pain causes a gradual and prolonged increase in plasma corticosterone level in 7-day-old male rats; twenty-four hours after injection of formalin, the basal corticosterone level still exceeds the initial basal corticosterone value. Chronic treatments of rat dams with buspirone before restraint stress during gestation normalize in the offspring pain-like behavior and induce during the acute phase in the formalin test the stronger corticosterone increase as compared to the stress hormonal elevation in animals with other prenatal treatments. Negative correlation between plasma corticosterone level and the number of flexes+shakes is revealed in buspirone+stress rats. The new data enhance the idea about relativity of the HPA axis hyporeactive period and suggest that maternal buspirone prior to stress during gestation may enhance an adaptive mechanism of the inflammatory nociceptive system in the infant male offspring through activation of the HPA axis peripheral link.

scholarly journals Vitamin A regulates hypothalamic–pituitary–adrenal axis status in LOU/C rats

2013 ◽  
Vol 219 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Nathalie Marissal-Arvy ◽  
Rachel Hamiani ◽  
Emmanuel Richard ◽  
Marie-Pierre Moisan ◽  
Véronique Pallet
Keyword(s):  
Vitamin A ◽  
Hpa Axis ◽  
Restraint Stress ◽  
Vitamin A Deficiency ◽  
Plasma Corticosterone ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosteroid Receptors ◽  
Vitamin A Status ◽  
Corticosterone Response ◽  
Hpa Axis Activity

The aim of this study was to explore the involvement of retinoids in the hypoactivity and hyporeactivity to stress of the hypothalamic–pituitary–adrenal (HPA) axis in LOU/C rats. We measured the effects of vitamin A deficiency administered or not with retinoic acid (RA) on plasma corticosterone in standard conditions and in response to restraint stress and on hypothalamic and hippocampal expression of corticosteroid receptors, corticotropin-releasing hormone and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in LOU/C rats. Interestingly, under control conditions, we measured a higher plasma concentration of retinol in LOU/C than in Wistar rats, which could contribute to the lower basal activity of the HPA axis in LOU/C rats. Vitamin A deficiency induced an increased HPA axis activity in LOU/C rats, normalized by RA administration. Compared with LOU/C control rats, vitamin A-deficient rats showed a delayed and heightened corticosterone response to restraint stress. The expression of corticosteroid receptors was strongly decreased by vitamin A deficiency in the hippocampus, which could contribute to a less efficient feedback by corticosterone on HPA axis tone. The expression of 11β-HSD1 was increased by vitamin A deficiency in the hypothalamus (+62.5%) as in the hippocampus (+104.7%), which could lead to a higher production of corticosterone locally and contribute to alteration of the hippocampus. RA supplementation treatment restored corticosterone concentrations and 11β-HSD1 expression to control levels. The high vitamin A status of LOU/C rats could contribute to their low HPA axis activity/reactivity and to a protective effect against 11β-HSD1-mediated deleterious action on cognitive performances during ageing.

scholarly journals Role of hypothalamic-pituitary adrenal-axis, toll-like receptors, and macrophage polarization in pre-atherosclerotic changes induced by social isolation stress in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Arvin Haj-Mirzaian ◽  
Kiana Ramezanzadeh ◽  
Siavash Shariatzadeh ◽  
Michael Tajik ◽  
Farima Khalafi ◽  
...  
Keyword(s):  
Social Isolation ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Macrophage Polarization ◽  
Toll Like Receptors ◽  
Isolation Stress ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Atherosclerotic Changes ◽  
Pituitary Adrenal Axis

AbstractIt has been well documented that chronic stress can induce atherosclerotic changes, however, the underlying mechanisms is yet to be established. In this regard, this study aimed to elucidate the relation between hypothalamic-pituitary adrenal-axis (HPA-axis), toll-like receptors (TLRs), as well as M1/M2 macrophage ratio and pre-atherosclerotic changes in social isolation stress (SIS) in mice. We used small interfering RNA against the glucocorticoid receptor (GR) to evaluate the relation between HPA-axis and TLRs. C57BL/6J mice were subjected to SIS and RT-PCR, ELISA, flow cytometry, and immunohistochemistry were used to assess the relations between pre-atherosclerotic changes and TLRs, macrophage polarization, pro-inflammatory cytokines, and cell adhesion molecules in aortic tissue. We used TAK-242 (0.3 mg/kg, intraperitoneally), a selective antagonist of TLR4, as a possible prophylactic treatment for atherosclerotic changes induced by SIS. We observed that isolated animals had higher serum concentration of corticosterone and higher body weight in comparison to normal animals. In isolated animals, results of in vitro study showed that knocking-down of the GR in bone marrow–derived monocytes significantly decreased the expression of TLR4. In vivo study suggested higher expression of TLR4 on circulating monocytes and higher M1/M2 ratio in aortic samples. Pathological study showed a mild pre-atherosclerotic change in isolated animals. Finally, we observed that treating animals with TAK-242 could significantly inhibit the pre-atherosclerotic changes. SIS can possibly increase the risk of atherosclerosis through inducing abnormal HPA-axis activity and subsequently lead to TLR4 up-regulation, vascular inflammation, high M1/M2 ratio in intima. Thus, TLR4 inhibitors might be a novel treatment to decrease the risk of atherosclerosis induced by chronic stress.

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