Tissue-specific modulation of glucocorticoid receptor expression in response to salinity acclimation in rainbow trout.

While studies clearly point to a role for cortisol signaling in seawater adaptation, very little is known about salinity impact on glucocorticoid receptor (GR) expression in fish. To this end, we investigated the temporal GR expression in the gill and liver of rainbow trout (Oncorhynchus mykiss) to salinity exposure. Trout were subjected to gradual salinity increases (11 ppt for 1 d, 17 ppt for 2 d and 23 ppt for 2 d) over a five day period.

Cortisol treatment affects glucocorticoid receptor and glucocorticoid-responsive genes in the liver of rainbow trout.

We investigated whether longer-term cortisol exposure modified hepatic glucocorticoid receptor (GR) status and tissue responsiveness to cortisol stimulation in rainbow trout. Fish were given intraperitoneal implants of cortisol (50mg/kg body mass) and this led to elevated plasma cortisol levels mimicking chronically stressed salmonids. There was significantly higher hepatic GR mRNA abundance, despite a drop in GR protein content in the liver of cortisol-treated fish.

Autoregulation of glucocorticoid receptor by cortisol in rainbow trout hepatocytes.

We used primary cultures of trout hepatocytes and a physiological dose of cortisol (100 ng/ml), mimicking stressed levels in salmonid fish, to address the impact of glucocorticoid stimulation on glucocorticoid receptor (GR) mRNA abundance and protein content. Cortisol significantly elevated GR mRNA content over a 24-h period; this increase was abolished by actinomycin D, suggesting transcriptional control of GR. However, cortisol significantly decreased GR protein content, leading us to hypothesize that lower GR protein content may be regulating GR mRNA abundance.