The CNS site of glucocorticoid negative feedback during LPS- and psychological stress-induced fevers

1996 ◽  
Vol 271 (3) ◽  
pp. R732-R737 ◽  
Author(s):  
L. E. Morrow ◽  
J. L. McClellan ◽  
J. J. Klir ◽  
M. J. Kluger
Keyword(s):  
Glucocorticoid Receptor ◽  
Dentate Gyrus ◽  
Receptor Antagonist ◽  
Open Field ◽  
Psychological Stress ◽  
Negative Feedback ◽  
Brain Regions ◽  
Type Ii ◽  
Neural Connections ◽  
Sites Of Action

Glucocorticoids exert negative feedback in the anterior hypothalamus (AH) during lipopolysaccharide (LPS)-induced fevers, but the central location of their negative feedback during psychological stress-induced fever has not been determined. To confirm that glucocorticoid modulation of LPS fever occurs in the AH, adrenalectomized animals were injected intrahypothalamically with either 0.25 ng of corticosterone or vehicle followed by 50 micrograms/kg LPS intraperitoneally. Animals pretreated with corticosterone developed significantly smaller fevers (P = 0.007) than animals given vehicle. To determine if glucocorticoid modulation during psychological stress-induced fever may occur in the hippocampus, the fornix was transected to block hippocampal communication with the AH. This resulted in significantly larger psychological stress-induced fevers (P = 0.02) compared with sham-operated animals. There were no differences between these groups for LPS-induced fevers (P = 0.92). To determine where in the hippocampus glucocorticoids might exert their negative feedback during psychological stress, rats were microinjected with either 1 ng RU-38486 (a type II glucocorticoid receptor antagonist) or vehicle into the dentate gyrus prior to exposure to the open field. There were no differences between the psychological stress-induced fevers of the RU-38486- and vehicle-injected groups, supporting the hypothesis that these fevers are modulated elsewhere in the hippocampus. Our data support the hypothesis that glucocorticoids modulate LPS-induced fever in the AH and do not involve the hippocampus, and that psychological stress-induced fevers are modulated by neural connections between the hippocampus and the hypothalamus. The precise sites of action of glucocorticoid negative feedback on stress-induced fevers in the hippocampus (or other brain regions) are not yet known.

Stress alters cutaneous permeability barrier homeostasis

2000 ◽  
Vol 278 (2) ◽  
pp. R367-R372 ◽  
Author(s):  
Mitsuhiro Denda ◽  
Toru Tsuchiya ◽  
Peter M. Elias ◽  
Kenneth R. Feingold
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Psychological Stress ◽  
Skin Disease ◽  
Barrier Function ◽  
Plasma Corticosterone ◽  
Permeability Barrier ◽  
Hairless Mice ◽  
Ru 486 ◽  
Kinetics Of

Recent studies have shown that psychological stress can influence cutaneous barrier function, suggesting that this form of stress could trigger or aggravate skin disease. In the present study, we demonstrate that transfer of hairless mice to a different cage delays barrier recovery rates. Pretreatment with a phenothiazine sedative, chlorpromazine, before transfer of animals restored the kinetics of barrier recovery toward normal, suggesting that psychological stress is the basis for this alteration in barrier homeostasis. To determine the mechanism linking psychological stress to altered barrier recovery, we first demonstrated that plasma corticosterone levels increase markedly after transfer of animals to new cages and that pretreatment with chlorpromazine blocks this increase. Second, we demonstrated that the systemic administration of corticosterone delays barrier recovery. Finally, we demonstrated that pretreatment with the glucocorticoid receptor antagonist RU-486 blocks the delay in barrier recovery produced by systemic corticosterone, change of cage, or immobilization. These results suggest that psychological stress stimulates increased production of glucocorticoids, which, in turn, adversely affects permeability barrier homeostasis.

Neonatal Handling Alters Adrenocortical Negative Feedback Sensitivity and Hippocampal Type II Glucocorticoid Receptor Binding in the Rat

1989 ◽  
Vol 50 (5) ◽  
pp. 597-604 ◽  
Author(s):  
Michael J. Meaney ◽  
David H. Aitken ◽  
Victor Viau ◽  
Shakti Sharma ◽  
Alain Sarrieau
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Binding ◽  
Negative Feedback ◽  
Type Ii ◽  
Neonatal Handling ◽  
Feedback Sensitivity

scholarly journals Effects of corticosteroids on urinary ammonium excretion in humans.

1994 ◽  
Vol 4 (8) ◽  
pp. 1531-1537
Author(s):  
M M Waybill ◽  
J N Clore ◽  
R A Emerick ◽  
C O Watlington ◽  
A C Schoolwerth
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Steroid Hormones ◽  
Serum Potassium ◽  
Mineralocorticoid Receptor ◽  
Normal Male ◽  
Type I ◽  
Ammonium Excretion ◽  
Type Ii ◽  
Selective Effects

This study was designed to examine the selective effects of glucocorticoid and mineralocorticoid classes of steroid hormones on urinary ammonium excretion in humans. In 22 10-day studies, normal male volunteers received either 9 alpha-fludrohydrocortisone or hydrocortisone, alone or with the receptor antagonist spironolactone or mifepristone. The small but significant increase in ammonium excretion noted with the administration of 9 alpha-fludrohydrocortisone was associated with a significant decrease in serum potassium. In contrast, a significantly larger increase in ammonium excretion was noted with hydrocortisone, without concomitant electrolyte changes. Spironolactone did not alter the effect on ammonium excretion by either corticosteroid, whereas mifepristone markedly blunted the hydrocortisone-induced increase in urinary ammonium excretion. It was concluded that glucocorticoids increase urinary ammonium excretion in humans and that this effect occurs through binding to the Type II (glucocorticoid) receptor rather than by cross-occupancy of the Type I (mineralocorticoid) receptor.

Central effects of glucocorticoid receptor antagonist RU-38486 on lipopolysaccharide and stress-induced fever

1994 ◽  
Vol 267 (3) ◽  
pp. R705-R711 ◽  
Author(s):  
J. L. McClellan ◽  
J. J. Klir ◽  
L. E. Morrow ◽  
M. J. Kluger
Keyword(s):  
Receptor Antagonist ◽  
Open Field ◽  
Intraperitoneal Injection ◽  
Plasma Corticosterone ◽  
Anterior Hypothalamus ◽  
Intracerebroventricular Injection ◽  
Type Ii ◽  
Central Effects ◽  
Lower Temperature ◽  
The Brain

Intracerebroventricular administration of the glucocorticoid type II receptor antagonist RU-38486 leads to an increased fever after injection of lipopolysaccharide (LPS) in awake unrestrained rats, indicating that endogenous glucocorticoids act centrally to lower temperature after the intraperitoneal injection of LPS. The current study examined where in the brain glucocorticoids exert these effects on fever and if these effects involve plasma interleukin-6 and corticosterone. RU-38486 injected intracerebroventricularly (10 ng/animal) led to a significantly greater rise in biotelemetered body temperature (BT) 120-240 min post-LPS (50 mg/kg ip) compared with controls (0.89 +/- 0.14 vs. 0.44 +/- 0.22 degree C, P = 0.0482), confirming our earlier study, and also led to a significantly greater rise in BT after exposure to an open field when the RU-38486 was infused intracerebroventricularly (10 ng/ml, 1 microliter/h) for 20 h before the exposure (1.48 +/- 0.18 vs. 1.06 +/- 0.11 degree C, P = 0.023). When rats were injected with RU-38486 into the anterior hypothalamus (1 ng/animal), there was an increased rise in BT after injection of LPS (1.74 +/- 0.27 vs. 0.82 +/- 0.22 degree C, P = 0.0075) but not after exposure to an open field (1 ng intrahypothalamically, 1 h preexposure). There were no differences in plasma interleukin (IL)-6-like activity or plasma corticosterone after intracerebroventricular injection of RU-38486 and intraperitoneal injection of LPS. We conclude that endogenous glucocorticoids are working centrally to modulate fever after LPS and exposure to open field, and that LPS-induced fever is modulated by glucocorticoids in the anterior hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Glucocorticoid receptor antagonist administration in a Cushing's syndrome model rat

2019 ◽  
Author(s):  
Toshiro Seki ◽  
Atsushi Yasuda ◽  
Natsumi Kitajima ◽  
Masami Seki ◽  
Masayuki Oki ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Cushing’S Syndrome ◽  
Cushing's Syndrome

scholarly journals Interleukin-1 receptor antagonist binds to the type II interleukin-1 receptor on B cells and neutrophils.

1991 ◽  
Vol 266 (30) ◽  
pp. 20311-20315 ◽  
Author(s):  
D.J. Dripps ◽  
E. Verderber ◽  
R.K. Ng ◽  
R.C. Thompson ◽  
S.P. Eisenberg
Keyword(s):  
B Cells ◽  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Type Ii ◽  
Interleukin 1 Receptor Antagonist

scholarly journals The influence of stress hormones and aggression on cooperative behaviour in subordinate meerkats

2017 ◽  
Vol 284 (1863) ◽  
pp. 20171248 ◽  
Author(s):  
Ben Dantzer ◽  
Ines Braga Goncalves ◽  
Helen C. Spence-Jones ◽  
Nigel C. Bennett ◽  
Michael Heistermann ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Treatment Effects ◽  
Stress Hormones ◽  
Cooperative Behaviour ◽  
Food Provisioning ◽  
Stress Hormone ◽  
Suricata Suricatta

In cooperative breeders, aggression from dominant breeders directed at subordinates may raise subordinate stress hormone (glucocorticoid) concentrations. This may benefit dominants by suppressing subordinate reproduction but it is uncertain whether aggression from dominants can elevate subordinate cooperative behaviour, or how resulting changes in subordinate glucocorticoid concentrations affect their cooperative behaviour. We show here that the effects of manipulating glucocorticoid concentrations in wild meerkats ( Suricata suricatta ) on cooperative behaviour varied between cooperative activities as well as between the sexes. Subordinates of both sexes treated with a glucocorticoid receptor antagonist (mifepristone) exhibited significantly more pup protection behaviour (babysitting) compared to those treated with glucocorticoids (cortisol) or controls. Females treated with mifepristone had a higher probability of exhibiting pup food provisioning (pup-feeding) compared to those treated with cortisol. In males, there were no treatment effects on the probability of pup-feeding, but those treated with cortisol gave a higher proportion of the food they found to pups than those treated with mifepristone. Using 19 years of behavioural data, we also show that dominant females did not increase the frequency with which they directed aggression at subordinates at times when the need for assistance was highest. Our results suggest that it is unlikely that dominant females manipulate the cooperative behaviour of subordinates through the effects of aggression on their glucocorticoid levels and that the function of aggression directed at subordinates is probably to reduce the probability they will breed.

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