Immunohistochemical localization of glucocorticoid receptors in the forebrain of the rainbow trout (Oncorhynchus mykiss)

Teitsma, Christine A.; Anglade, Isabelle; Toutirais, Géraldine; Muñoz‐cueto, José‐antonio; Saligaut, Dany; Ducouret, B.; Kah, Olivier

doi:10.1002/(sici)1096-9861(19981123)401:3<395::aid-cne7>3.0.co;2-p

Cited by 55 publications

(37 citation statements)

References 67 publications

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“…Sandor et al 1984, Weisbart et al 1984, Maule & Schreck 1990, Pottinger & Moore 1997, Weyts et al 1998, Marsigliante et al 2000, and full-length glucocorticoids receptor (GR) cDNAs (rainbow trout (Oncorhynchus mykiss): Ducouret et al (1995), Takeo et al (1996); Japanese flounder, Genbank ABO1344) and a partial tilapia GR cDNA (Tagawa et al 1997) have been cloned. Expression of rainbow trout GR (rtGR) transcript is found in a number of tissues (Ducouret et al 1995, Takeo et al 1996, is widely distributed in the brain (Teitsma et al 1997(Teitsma et al , 1998 and has been identified in gill chloride cells (Uchida et al 1998), the cells believed to be responsible for branchial ion movement (Perry 1997). Despite the absence of aldosterone in fish, a recent study identified a partial cDNA sequence of a corticosteroid receptor in rainbow trout, whose amino acid sequence showed a high homology with known mineralocorticoid receptors (MRs).…”

Section: Introductionsupporting

confidence: 92%

Evidence for two distinct functional glucocorticoid receptors in teleost fish

Bury¹,

Sturm²,

Rouzic³

et al. 2003

Journal of Molecular Endocrinology

232

178

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Using RT-PCR with degenerated primers followed by screening of a rainbow trout (Oncorhynchus mykiss) intestinal cDNA library, we have isolated from the rainbow trout a new corticosteroid receptor which shows high sequence homology with other glucocorticoid receptors (GRs), but is clearly different from the previous trout GR (named rtGR1). Phylogenetic analysis of these two sequences and other GRs known in mammals, amphibians and fishes indicate that the GR duplication is probably common to most teleost fish. The open reading frame of this new trout GR (named rtGR2) encodes a protein of 669 amino acids and in vitro translation produces a protein of 80 kDa that appears clearly different from rtGR1 protein (88 kDa). Using rtGR2 cDNA as a probe, a 7·3 kb transcript was observed in various tissues suggesting that this gene would lead to expression of a steroid receptor. In vitro studies were used to further characterize this new corticosteroid receptor. Binding studies with recombinant rtGR1 and rtGR2 proteins show that the two receptors have a similar affinity for dexamethasone (GR1 K d =5·05±0·45 nM; GR2 K d =3·04±0·79 nM). Co-transfection of an rtGR1 or rtGR2 expression vector into CHO-K1 or COS-7 cells, along with a reporter plasmid containing multiple consensus glucocorticoid response elements, shows that both clones are able to induce transcriptional activity in the presence of cortisol and dexamethasone. Moreover, at 10 −6 M 11-deoxycortisol and corticosterone partially induced rtGR2 transactivation activity but were without effect on rtGR1. The other major teleost reproductive hormones, as well as a number of their precursors or breakdown products of these and corticosteroid hormones, were without major effects on either receptor. Interestingly, rtGR2 transactivational activity was induced at far lower concentrations of dexamethasone or cortisol (cortisol EC 50 =0·72±0·87 nM) compared with rtGR1 (cortisol EC 50 =46±12 nM). Similarly, even though RU486 inhibited transactivation activity in both rtGR1 and rtGR2, rtGR1 was more sensitive to this GR antagonist. Altogether, these results indicate that these two GR sequences encode for two functionally distinct GRs acting as ligand-inducible transcription factors in rainbow trout.

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Section: Introductionsupporting

confidence: 92%

Evidence for two distinct functional glucocorticoid receptors in teleost fish

Bury¹,

Sturm²,

Rouzic³

et al. 2003

Journal of Molecular Endocrinology

232

178

View full text Add to dashboard Cite

show abstract

“…In teleosts, cortisol can act as a mineralocorticoid and glucocorticoid, targeting both glucocorticoid receptor(s) (GR) and mineralocorticoid (Arai, Assil et al) receptors(s) (Knoebl, Fitzpatrick et al 1996;Teitsma, Anglade et al 1998;Greenwood, Butler et al 2003;Sturm, Bury et al 2005). Under normal circumstances, cortisol release is associated with stress, gluconeogenisis, metabolic function, immune suppression, and osmoregulation in several species of fish.…”

Section: Understanding the Role Of Chronic Stress Response In Semelpacontrasting

confidence: 78%

Seasonal changes in CRF-I and urotensin I transcript levels in masu salmon: Correlation with cortisol secretion during spawning

Westring

Ando

Kitahashi

et al. 2008

General and Comparative Endocrinology

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Pacific salmon employ a semelparous reproductive strategy where sexual maturation is followed by rapid senescence and death. Cortisol overproduction has been implicated as the central physiologic event responsible for the post-spawning demise of these fish. Cortisol homeostasis is regulated through the action of hormones of the hypothalamus-pituitary-interrenal (HPI) axis. These include corticotropin-releasing factor (CRF) and urotensin-I (UI). In the present study, masu salmon (Oncorhynchus masou) were assayed for changes in the levels CRF-I and UI mRNA transcripts by quantitative real-time PCR (qRT-PCR). These results were compared to plasma cortisol levels in juvenile, adult, and spawning masu salmon to identify specific regulatory factors that appear to be functionally associated with changes in cortisol levels. Intramuscular implantation of GnRH analog (GnRHa) capsules was also used to determine whether GnRH influences stress hormone levels. In both male and female masu salmon, spawning fish experienced a 5-7 fold increase in plasma cortisol levels relative to juvenile non-spawning salmon. Changes in CRF-I mRNA levels were characterized by 1-2 distinctive short-term surges in adult masu salmon. Conversely, seasonal changes in UI mRNA levels displayed broad and sustained increases during the pre-spawning and spawning periods. The increases in UI mRNA levels were positively correlated (R 2 = 0.21 male and 0.26 female, p<0.0001) with levels of plasma cortisol in the pre-spawning and spawning periods. Despite the importance of GnRH in sexual maturation and reproduction, the administration of GnRHa to test animals failed to produce broad changes in CRF-I, UI or plasma cortisol levels. These findings suggest a more direct role for UI than for CRF-I in the regulation of cortisol levels in spawning Pacific salmon.

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“…Moreover, we provide novel evidence that the negative feedback effects of cortisol on plasma ACTH can persist for at least 8 days beyond the return of cortisol to baseline levels. In contrast, although cortisol has been shown to decrease POA crf gene expression in a few fish species (reviewed by Bernier et al 2009), and NPO CRF immunoreactive neurons co-express GRs in rainbow trout (Teitsma et al 1998), chronically elevated cortisol levels in this study were associated with a sustained increase in POA crf mRNA levels. Similarly, suppression of GR signaling in rainbow trout using the GR antagonist RU486 reduces POA crf mRNA levels (Doyon et al 2006, Alderman et al 2012.…”

Section: Discussionmentioning

confidence: 99%

Chronic cortisol and the regulation of food intake and the endocrine growth axis in rainbow trout

Madison

Tavakoli

Krämer

et al. 2015

Journal of Endocrinology

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To gain a better understanding of the mechanisms by which cortisol suppresses growth during chronic stress in fish, we characterized the effects of chronic cortisol on food intake, mass gain, the expression of appetite-regulating factors, and the activity of the GH/IGF axis. Fish given osmotic pumps that maintained plasma cortisol levels at w70 or 116 ng/ml for 34 days were sampled 14, 28 and 42 days post-implantation. Relative to shams, the cortisol treatments reduced food intake by 40-60% and elicited marked increases in liver leptin (lep-a1) and brain preoptic area (POA) corticotropin-releasing factor (crf) mRNA levels. The cortisol treatments also elicited 40-80% reductions in mass gain associated with increases in pituitary gh, liver gh receptor (ghr), liver igfI and igf binding protein (igfbp)-1 and -2 mRNA levels, reduced plasma GH and no change in plasma IGF1. During recovery, while plasma GH and pituitary gh, liver ghr and igfI gene expression did not differ between treatments, the high cortisol-treated fish had lower plasma IGF1 and elevated liver igfbp1 mRNA levels. Finally, the cortisol-treated fish had higher plasma glucose levels, reduced liver glycogen and lipid reserves, and muscle lipid content. Thus, our findings suggest that the growth-suppressing effects of chronic cortisol in rainbow trout result from reduced food intake mediated at least in part by increases in liver lep-a1 and POA crf mRNA, from sustained increases in hepatic igfbp1 expression that reduce the growth-promoting actions of the GH/IGF axis, and from a mobilization of energy reserves.

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Immunohistochemical localization of glucocorticoid receptors in the forebrain of the rainbow trout (Oncorhynchus mykiss)

Cited by 55 publications

References 67 publications

Evidence for two distinct functional glucocorticoid receptors in teleost fish

Evidence for two distinct functional glucocorticoid receptors in teleost fish

Seasonal changes in CRF-I and urotensin I transcript levels in masu salmon: Correlation with cortisol secretion during spawning

Chronic cortisol and the regulation of food intake and the endocrine growth axis in rainbow trout

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