The Hypothalamus and Adrenal Regulate Modulation of Corticosterone Release in Redpolls (Carduelis flammea—An Arctic-Breeding Song Bird)

Abstract The functional relationship between thyroid, adrenal and gonadal hormones was investigated using adult male rats. Hypothyroidism was produced by the administration of 4-methyl-2-thiouracil (thiouracil) in the drinking water for 2 weeks. Plasma concentrations of TSH dramatically increased, whereas plasma concentrations of tri-iodothyronine and thyroxine decreased in thiouracil-treated rats as compared with euthyroid rats. Hypothyroidism increased basal levels of plasma ACTH and pituitary content of ACTH. The pituitary responsiveness to CRH for ACTH release markedly increased, whereas the adrenal responsiveness to ACTH for corticosterone release decreased. These results indicated that hypothyroidism causes adrenal dysfunction in adult male rats. Pituitary contents of LH and prolactin decreased in hypothyroid rats as compared with euthyroid rats. In addition, hypothyroidism lowered pituitary LH responsiveness to LHRH. Testicular responsiveness to human chorionic gonadotrophin for testosterone release, however, was not different between euthyroid and hypothyroid animals. These results indicated that hypothyroidism causes adrenal dysfunction and results in hypersecretion of ACTH from the pituitary gland. Adrenal dysfunction may contribute to the inhibition of LHRH secretion from the hypothalamus, possibly mediated by excess CRH. Journal of Endocrinology (1997) 152, 147–154

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Hypothalamic-pituitary-adrenal axis changes allow seasonal modulation of corticosterone in a bird

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.5.r1338 ◽

1998 ◽

Vol 274 (5) ◽

pp. R1338-R1344 ◽

Cited By ~ 39

Author(s):

L. Michael Romero ◽

Kiran K. Soma ◽

John C. Wingfield

Keyword(s):

Hypothalamic Pituitary Adrenal Axis ◽

Corticotropin Releasing Factor ◽

Arginine Vasotocin ◽

Free Living ◽

Hypothalamic Pituitary Adrenal ◽

Adrenal Axis ◽

Maximal Output ◽

Calcarius Lapponicus ◽

Corticosterone Release ◽

Pituitary Adrenal Axis

We examined possible mechanisms underlying seasonal stress modulation in Lapland longspurs ( Calcarius lapponicus), a species that breeds and molts (the energetically costly replacement of feathers) in the Alaskan Arctic. Free-living Lapland longspurs show dramatically reduced maximal corticosterone release during molt compared with the breeding season, an effect lost in captive birds. Neither changes in corticosterone binding proteins nor the overall condition of the bird (assessed by weight and fat storage) can explain different seasonal corticosterone responses. Adrenal insensitivity also does not fully explain reduced maximal output because exogenous ACTH enhanced corticosterone release during molt. Exogenous ACTH in molting birds, however, cannot stimulate corticosterone to stress-induced levels during breeding, implying reduced adrenal capacity. Lapland longspur pituitaries appeared to respond to exogenous corticotropin-releasing factor, arginine vasotocin, and mesotocin (the avian equivalents of arginine vasopressin and oxytocin) during molt, suggesting that a mechanism upstream of the pituitary blunts corticosterone release. Taken together, these results indicate that seasonal modulation of corticosterone release in this species is controlled at multiple sites in the hypothalamic-pituitary-adrenal axis.

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Chronic intracerebroventricular CRF infusion attenuates ACTH-corticosterone release

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.255.2.e213 ◽

1988 ◽

Vol 255 (2) ◽

pp. E213-E217 ◽

Cited By ~ 3

Author(s):

J. J. Cunningham ◽

P. A. Meara ◽

R. Y. Lee ◽

H. H. Bode

Keyword(s):

Nervous System ◽

Adrenocorticotropic Hormone ◽

Feedback Mechanism ◽

Receptor Desensitization ◽

Negative Feedback Mechanism ◽

Corticosterone Secretion ◽

Acute Responses ◽

The Central Nervous System ◽

Corticosterone Release ◽

Pituitary Adrenal Axis

Bolus intracerebroventricular delivery of corticotropin-releasing factor (CRF) elicits acute responses of both the pituitary-adrenal axis and the sympathetic nervous system. We examined whether these stresslike responses could be maintained over a period of days by central delivery of CRF in nonstressed rats, as would be predicted if this peptide participates in the central nervous system regulation of chronic stress. CRF (4.3 or 21.5 micrograms/day) was continuously delivered into the cerebral ventricle via Alzet minipumps. In contrast to saline-infused controls, rats receiving CRF exhibited elevated excretions of corticosterone, norepinephrine, and urea nitrogen for several days. Thereafter, an attenuation of CRF responsiveness occurred when corticosterone excretion returned to basal levels despite continued central CRF infusion. However, CRF delivered intravenously during attenuation stimulated adrenocorticotropic hormone and corticosterone secretion, implicating a hypothalamic rather than pituitary locus for central CRF resistance. The present data do not permit a conclusion on whether the attenuation of the CRF response with time is the result of an ultrashort-loop negative-feedback mechanism or CRF receptor desensitization.

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Regulation of CRH-induced secretion of ACTH and corticosterone by SOM230 in rats

Acta Endocrinologica ◽

10.1530/eje.1.01998 ◽

2005 ◽

Vol 153 (3) ◽

pp. R7-R10 ◽

Cited By ~ 36

Author(s):

A P Silva ◽

P Schoeffter ◽

G Weckbecker ◽

C Bruns ◽

H A Schmid

Keyword(s):

Adrenocorticotropic Hormone ◽

Plasma Concentrations ◽

Inhibitory Effect ◽

Corticotropin Releasing Hormone ◽

Acth Secretion ◽

Releasing Hormone ◽

Corticosterone Secretion ◽

Corticosterone Release ◽

Acth Release

Objective: Adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome is biochemically characterized by increased plasma concentrations of ACTH inducing hypersecretion of cortisol. Somatostatin is known to inhibit ACTH secretion, and in vitro data have shown the inhibition of ACTH secretion by agonists activating sst2 and sst5 receptors. The present study aimed to determine the inhibitory effect of the multireceptor ligand SOM230, compared with the sst2-preferring agonist octreotide, on corticotropin-releasing hormone (CRH)-stimulated secretion of ACTH and corticosterone in rats. Methods: Secretion of ACTH and corticosterone was induced by i.v. application of CRH (0.5 μg/kg) in rats pretreated 1 h before by i.v. application of SOM230 (1, 3, or 10 μg/kg), octreotide (10 μg/kg) or NaCl 0.9%. Results: SOM230 (3 and 10 μg/kg) inhibited CRH-induced ACTH release by 45±3% and 51±2%, respectively, and corticosterone release by 43±5% and 27±16%, respectively. 10 μg/kg of octreotide tended to be less potent at inhibiting ACTH release (34±6% inhibition) and did not alter the secretion of corticosterone. Conclusion: SOM230 has a stronger inhibitory effect on ACTH and corticosterone secretion than octreotide in rats. This difference can be explained by its higher affinity to sst1, sst3 and especially sst5 receptors compared with octreotide.

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