Central and peripheral glucocorticoid receptors are involved in the plasma cortisol response to an acute stressor in rainbow trout

2012 ◽  
Vol 176 (1) ◽  
pp. 79-85 ◽  
Author(s):  
Sarah L. Alderman ◽  
Alison McGuire ◽  
Nicholas J. Bernier ◽  
Mathilakath M. Vijayan
Keyword(s):  
Rainbow Trout ◽  
Plasma Cortisol ◽  
Glucocorticoid Receptors ◽  
Cortisol Response ◽  
Acute Stressor

Differential expression of corticosteroid receptor genes in rainbow trout (Oncorhynchus mykiss) immune system in response to acute stress

2007 ◽  
Vol 64 (10) ◽  
pp. 1382-1389 ◽  
Author(s):  
Takashi Yada ◽  
Teruo Azuma ◽  
Susumu Hyodo ◽  
Tetsuya Hirano ◽  
E Gordon Grau ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Plasma Cortisol ◽  
Glucocorticoid Receptors ◽  
Acute Stress ◽  
Mrna Levels ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Corticosteroid Receptor ◽  
Polymerase Chain ◽  
Peripheral Blood Leucocytes

Expression of distinct corticosteroid receptor genes, glucocorticoid receptors 1 and 2 (GR-1 and GR-2, respectively) and mineralcorticoid receptor (MR), was quantified by real-time polymerase chain reaction (PCR) in peripheral blood leucocytes (PBL), spleen, and gill of rainbow trout (Oncorhynchus mykiss) after an acute netting stress. Plasma cortisol levels were significantly increased 2 h after stress and returned to prestress levels within 24 h. Consistent with changes in plasma cortisol, GR-2 mRNA levels in PBL increased significantly at 2 h after stress, returning to initial levels by 8 h. In contrast, GR-1 and MR levels in PBL decreased significantly at 24 h after stress, and these reduced levels were maintained for 7 days. Splenic mRNA levels of GR-1 and GR-2 also decreased at 8 h and 24 h after stress, returning to control levels by 7 days, whereas no significant change was observed in MR. In gill, there was no obvious change in corticosteroid receptor mRNA levels after stress, except for a transient decrease at 8 h in MR. These results suggest a variety of roles for the three corticosteroid receptors during immunosuppression in response to acute stress in trout.

scholarly journals Quantitative trait loci for magnitude of the plasma cortisol response to confinement in rainbow trout

2014 ◽  
Vol 45 (2) ◽  
pp. 223-234 ◽  
Author(s):  
E. Quillet ◽  
F. Krieg ◽  
N. Dechamp ◽  
C. Hervet ◽  
A. Bérard ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Trait Loci

Rapid cortisol signaling in response to acute stress involves changes in plasma membrane order in rainbow trout liver

2013 ◽  
Vol 304 (11) ◽  
pp. E1157-E1166 ◽  
Author(s):  
Laura Dindia ◽  
Erin Faught ◽  
Zoya Leonenko ◽  
Raymond Thomas ◽  
Mathilakath M. Vijayan
Keyword(s):  
Plasma Membrane ◽  
Rainbow Trout ◽  
Signaling Pathways ◽  
Membrane Fluidity ◽  
Plasma Cortisol ◽  
Acute Stress ◽  
Plasma Cortisol Level ◽  
Cellular Stress Response ◽  
Membrane Order ◽  
Acute Stressor

The activation of genomic signaling in response to stressor-mediated cortisol elevation has been studied extensively in teleosts. However, very little is known about the rapid signaling events elicited by this steroid. We tested the hypothesis that cortisol modulates key stress-related signaling pathways in response to an acute stressor in fish liver. To this end, we investigated the effect of an acute stressor on biophysical properties of plasma membrane and on stressor-related protein phosphorylation in rainbow trout ( Oncorhynchus mykiss) liver. A role for cortisol in modulating the acute cellular stress response was ascertained by blocking the stressor-induced elevation of this steroid by metyrapone. The acute stressor exposure increased plasma cortisol levels and liver membrane fluidity (measured by anisotropy of 1,6-diphenyl-1,3,5-hexatriene), but these responses were abolished by metyrapone. Atomic force microscopy further confirmed biophysical alterations in liver plasma membrane in response to stress, including changes in membrane domain topography. The changes in membrane order did not correspond to any changes in membrane fatty acid components after stress, suggesting that changes in membrane structure may be associated with cortisol incorporation into the lipid bilayer. Plasma cortisol elevation poststress correlated positively with activation of intracellular stress signaling pathways, including increased phosphorylation of extracellular signal-related kinases as well as several putative PKA and PKC but not Akt substrate proteins. Together, our results indicate that stressor-induced elevation of plasma cortisol level is associated with alterations in plasma membrane fluidity and rapid activation of stress-related signaling pathways in trout liver.

Is plasma cortisol response to stress in rainbow trout regulated by catecholamine-induced hyperglycemia?

2014 ◽  
Vol 205 ◽  
pp. 207-217 ◽  
Author(s):  
Manuel Gesto ◽  
Cristina Otero-Rodiño ◽  
Marcos A. López-Patiño ◽  
Jesús M. Míguez ◽  
José L. Soengas ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Response To Stress

scholarly journals Duress without stress: Cryptobia infection results in HPI axis dysfunction in rainbow trout

2013 ◽  
Vol 218 (3) ◽  
pp. 287-297 ◽  
Author(s):  
Barry N Madison ◽  
Patrick T K Woo ◽  
Nicholas J Bernier
Keyword(s):  
Gene Expression ◽  
Rainbow Trout ◽  
Plasma Cortisol ◽  
Head Kidney ◽  
Infected Fish ◽  
Control Fish ◽  
Cortisol Response ◽  
Mrna Levels ◽  
Air Exposure ◽  
Hpi Axis

Despite clear physiological duress, rainbow trout (Oncorhynchus mykiss) infected with the pathogenic haemoflagellateCryptobia salmositicado not appear to mount a cortisol stress response. Therefore, we hypothesized that the infection suppresses the stress response by inhibiting the key effectors of the hypothalamic–pituitary–interrenal (HPI) axis. To test this, we characterized the basal activity of the HPI axis and the cortisol response to air exposure in saline- and parasite-injected fish. All fish were sampled at 4 and 6 weeks post-injection (wpi). While both the treatment groups had resting plasma cortisol levels, the parasite-infected fish had lower levels of plasma ACTH than the control fish. Relative to the control fish, the infected fish had higher mRNA levels of brain pre-optic area corticotrophin-releasing factor (CRF) and pituitary CRF receptor type 1, no change in pituitary POMC-A1, -A2 and -B gene expression, higher and lower head kidney melanocortin 2 receptor mRNA levels at 4 and 6 wpi respectively and reduced gene expression of key proteins regulating interrenal steroidogenesis: StAR, cytochrome P450scc and 11β-hydroxylase. The parasite-infected fish also had a reduced plasma cortisol response to a 60-s air exposure stressor. Superfusion of the head kidney tissues of the parasite-infected fish led to significantly lower ACTH-stimulated cortisol release rates than that observed in the control fish. These novel findings show that infection of rainbow trout withC. salmositicaresults in complex changes in the transcriptional activity of both central and peripheral regulators of the HPI axis and in a reduction in the interrenal capacity to synthesize cortisol.

Biological activity of adrenocorticotropic hormone precursors on ovine adrenal cells

1995 ◽  
Vol 268 (4) ◽  
pp. E623-E629 ◽  
Author(s):  
J. Schwartz ◽  
F. Kleftogiannis ◽  
R. Jacobs ◽  
G. D. Thorburn ◽  
S. R. Crosby ◽  
...  
Keyword(s):  
Biological Activity ◽  
Plasma Cortisol ◽  
Inhibitory Action ◽  
Adrenocorticotropic Hormone ◽  
Physiological Role ◽  
Cortisol Response ◽  
Adrenal Cells ◽  
Fetal Cells ◽  
Fetal Plasma ◽  
Cortisol Responses

Adrenocorticotropic hormone (ACTH) is synthesized in the corticotrophs as a precursor, pro-opiomelanocortin (POMC), which is processed via proACTH to ACTH. Both precursors and ACTH are secreted. Although the steroidogenic activity of ACTH is well characterized, that of the precursors is not. This study assessed the capacity of POMC and proACTH to alter cortisol synthesis. POMC and proACTH were prepared by subjecting medium, conditioned by exposure to DMS-79 cells, to Sephadex chromatography, and the bioactivity was assessed in cultured-dissociated ovine adrenal cells. Alone neither POMC (< or = 2.6 nM) nor proACTH (< or = 0.7 nM) showed any consistent acute (6 h) stimulatory or inhibitory action on cortisol in either fetal or adult cells. In contrast, in fetal cells the precursors inhibited steroidogenic response to ACTH-(1-24). POMC at 2.6 nM, but not lower concentrations, decreased the cortisol responses to 0.01, 0.1, and 1 nM ACTH by at least 50%. ProACTH (0.70 and 0.23 nM) decreased the responses to ACTH at 0.01 nM by 89 and 67%, respectively, and at 0.1 nM by 49 and 34%, respectively. At 1 nM ACTH only 0.7 nM proACTH decreased the response to ACTH (by 69%). In contrast, in adult adrenal cells, the precursors did not significantly reduce the response to ACTH (range 0.01-1 nM). Therefore, these data indicate that POMC and proACTH can inhibit the cortisol response to ACTH in fetal adrenal cells, an effect that is concentration dependent. The data suggest that precursors may play a physiological role, possibly regulating fetal plasma cortisol concentrations.

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