Effects Of Exogenous Cortisol Research Articles

The effects of exogenous cortisol on myostatin transcription in rainbow trout, Oncorhynchus mykiss

Glucocorticoids (GCs) strongly regulate myostatin expression in mammals via glucocorticoid response elements (GREs), and bioinformatics methods suggest that this regulatory mechanism is conserved among many vertebrates. However, the multiple myostatin genes found in some fishes may be an exception. In silico promoter analyses of the three putative rainbow trout (Oncorhynchus mykiss) myostatin promoters have failed to identify putative GREs, suggesting a divergence in myostatin function. Therefore, we hypothesized that myostatin mRNA expression is not regulated by glucocorticoids in rainbow trout. In this study, both juvenile rainbow trout and primary trout myoblasts were treated with cortisol to examine the effects on myostatin mRNA expression. Results suggest that exogenous cortisol does not regulate myostatin-1a and -1b expression in vivo, as myostatin mRNA levels were not significantly affected by cortisol treatment in either red or white muscle tissue. In red muscle, myostatin-2a levels were significantly elevated in the cortisol treatment group relative to the control, but not the vehicle control, at both 12h and 24h post-injection. As such, it is unclear if cortisol was acting alone or in combination with the vehicle. Cortisol increased myostatin-1b expression in a dose-dependent manner in vitro. Further work is needed to determine if this response is the direct result of cortisol acting on the myostatin-1b promoter or through an alternative mechanism. These results suggest that regulation of myostatin by cortisol may not be as highly conserved as previously thought and support previous work that describes potential functional divergence of the multiple myostatin genes in fishes.

Effects of exogenous cortisol and seawater adaptation on thyroid hormone receptors in the smolt stage of the sockeye salmon, Oncorhynchus nerka

The objective of this investigation was to quantify how thyroid hormone receptors of the sockeye salmon, Oncorhynchus nerka, respond to salinity changes from freshwater (FW) to seawater (SW) conditions. Thy- roid hormone receptors (TRs) mRNA and protein expres- sions levels significantly increased when the fish were transferred from FW to SW, and the plasma T3 and T4 levels were significantly highest at 50 % SW and then maintained as control. Moreover, these parameters were significantly lower in the cortisol-injected groups than in the control. Hence, TRs, T3, and T4 may play a role in SW adaptation, when the fish migrate from FW to SW envi- ronments. We showed a negative correlation between cortisol and thyroid hormone levels, and a significant increase in plasma K ? levels in the kidney when the fish were transferred to SW, with levels being significantly lower in the cortisol-injected group. Hence, cortisol appears to be a stress hormone, and the plasma Na ? and Cl - levels significantly increased when the fish were transferred to SW, with levels being significantly lower in the cortisol- injected group. These results indicate that cortisol modu- lates ion transportation in the plasma.

The effect of exogenous cortisol during sleep on the behavioral and neural correlates of emotional memory consolidation in humans

A host of animal work demonstrates that the retention benefit for emotionally aversive over neutral memories is regulated by glucocorticoid action during memory consolidation. Particularly, glucocorticoids may affect systems-level processes that promote the gradual reorganization of emotional memory traces. These effects remain largely uninvestigated in humans. Therefore, in this functional magnetic resonance imaging study we administered hydrocortisone during a polysomnographically monitored night of sleep directly after healthy volunteers studied negative and neutral pictures in a double-blind, placebo-controlled, between-subjects design. The following evening memory consolidation was probed during a recognition memory test in the MR scanner by assessing the difference in brain activity associated with memory for the consolidated items studied before sleep and new, unconsolidated items studied shortly before test (remote vs. recent memory paradigm). Hydrocortisone administration resulted in elevated cortisol levels throughout the experimental night with no group difference at recent encoding or test. Behaviorally, we showed that cortisol enhanced the difference between emotional and neutral consolidated memory, effectively prioritizing emotional memory consolidation. On a neural level, we found that cortisol reduced amygdala reactivity related to the retrieval of these same consolidated, negative items. These findings show that cortisol administration during first post-encoding sleep had a twofold effect on the first 24h of emotional memory consolidation. While cortisol prioritized recognition memory for emotional items, it reduced reactivation of the neural circuitry underlying emotional responsiveness during retrieval. These findings fit recent theories on emotional depotentiation following consolidation during sleep, although future research should establish the sleep-dependence of this effect. Moreover, our data may shed light on mechanisms underlying potential therapeutic effects of cortisol administration following psychological trauma.

Effects of exogenous cortisol on the GH/IGF-I/IGFBP network in channel catfish

Glucocorticoids are known to hinder somatic growth in a number of vertebrate species. In order to better understand the mechanisms through which they may act in channel catfish, we examined the effects of feeding cortisol on the growth hormone (GH)/insulin-like growth factor-I (IGF-I)/IGF-binding protein (IGFBP) network. Fish (30.6 ± 3.0 g) were fed once daily for 4 weeks and treatments included: (1) High-cortisol (dietary cortisol provided at 400 mg/kg feed), (2) Low-cortisol (dietary cortisol provided at 200 mg/kg feed), and (3) Control (commercial catfish feed). Fish fed diets with cortisol weighed approximately 50% less than Controls. Feed intake was reduced by approximately 30% in both treatments of cortisol fed fish compared to Controls. A ∼20-kDa IGFBP was observed in plasma from High- and Low-treated fish while it was not detected in Control fish plasma. High-cortisol treatment increased pituitary GH mRNA expression approximately 10-fold while liver IGF-I mRNA expression was not different between cortisol-treated fish and Controls. Cortisol treatments decreased plasma levels of IGF-I. These data indicate that feeding cortisol for 4 weeks reduces weight gain, feed intake, and plasma levels of IGF-I and induces a ∼20-kDa IGFBP. One mechanism through which cortisol may impede growth of catfish is through an increase in a low molecular weight IGFBP which may lead to inhibitory effects on the action of IGF-I.

Effect of cortisol on some osmoregulatory parameters of the teleost, Oreochromis niloticus L., after transference from freshwater to seawater

This trial was conducted in order to determine the effects of cortisol on salt water acclimation of tilapia Oreochromis niloticus (L.). Tilapia (n=42) were injected intraperitoneally with cortisol and then were directly transferred from freshwater (FW) to 15‰ salt water (SW). Changes in plasma osmolality, chloride ion concentration (Cl-), plasma level of cortisol and gill Na+, K+-ATPase activity were measured at 6, 12, 24, 48, 72 and 168 hours after transference to 15‰ SW. Plasma osmolality and Cl- increased immediately after transference until 12-24 h. The fish injected with cortisol (F) showed higher plasma levels of cortisol than those from control group (C) that maintained the initial levels during the experiment. Gill Na+, K+-ATPase activity of C fish began to increase at first hours after transference and peak at 48h. The differences between gill Na+, K+-ATPase activity of F and C groups were significant (P<0.05) in FW, which confirm the effect of exogenous cortisol.

In vitro effects of environmental salinity and cortisol on chloride cell differentiation in embryos of Mozambique tilapia, Oreochromis mossambicus, measured using a newly developed 'yolk-ball' incubation system.

To examine the functional differentiation of chloride cells in the yolk-sac membrane of tilapia (Oreochromis mossambicus) embryos, we developed a 'yolk-ball' incubation system in which the yolk sac was separated from the embryonic body and subjected to incubation in vitro. The yolk-ball preparation consists of the yolk and the covering yolk-sac membrane, which contains a rich population of chloride cells. After appropriate cutting, the incision on the yolk ball healed during incubation in balanced salt solution for 3h, so that the yolk-sac membrane completely enclosed the yolk. Yolk balls prepared from freshwater-acclimated embryos were transferred either to fresh water or to sea water and incubated for 48 and 96 h to elucidate the morphological changes in the chloride cells in response to environmental salinity. The chloride cells in the yolk-sac membrane were larger in sea water than in fresh water. In yolk balls transferred to sea water, chloride cells often formed multicellular complexes characteristic of seawater-type chloride cells. In those transferred to fresh water, however, the cells were small and rarely formed such complexes. These responses of chloride cells were identical to those observed in intact embryos. Thus, chloride cells in the yolk-sac membrane could differentiate into the seawater type independent of the embryonic body. To examine the possible effects of exogenous cortisol on chloride cell differentiation, the yolk balls were incubated for 48 h in fresh water or sea water containing different doses of cortisol (0.1-10 microg x ml(-1)). Although chloride cells were consistently larger in sea water than in fresh water in all experimental groups, cortisol administration had no effect on chloride cell surface area in either medium. These findings indicate that the chloride cells in the yolk-sac membrane are equipped with an autonomous mechanism of functional differentiation that is independent of the embryonic endocrine and nervous systems. The yolk-ball incubation system established here is an excellent experimental model for further studies on chloride cell differentiation and function.

Effects of cortisol and salinity challenge on water balance in developing larvae of tilapia (Oreochromis mossambicus).

Effects of exogenous cortisol on drinking rate and water content in developing larvae of tilapia (Oreochromis mossambicus) were examined. Both freshwater- and seawater-adapted larvae showed increases in drinking rates with development. Drinking rates of seawater-adapted larvae were about four- to ninefold higher than those of freshwater-adapted larvae from day 2 to day 5 after hatching. Seawater-adapted larvae showed declines in drinking rate and water content at 4 and 14 h, respectively, after immersion in 10 mg L(-1) cortisol. In the case of freshwater-adapted larvae, the drinking rate decreased after 8 h of cortisol immersion, while the water content did not show a significant change even after 32 h of cortisol immersion. In a subsequent experiment of transfer from freshwater to 20 ppt (parts per thousand, salinity) seawater, immersion in 10 mg L(-1) cortisol for 8-24 h enhanced the drinking rate in larvae at 4 h after transfer, but no significant difference was found in water contents between cortisol-treated and control groups following transfer. These results suggest that cortisol is involved in the regulation of drinking activity in developing tilapia larvae.

Cortisol infusion depresses the ratio of bioactive to immunoreactive ACTH in adrenalectomized sheep fetuses.

We examined the effects of exogenous cortisol on plasma immunoreactive adrenocorticotropic hormone (iACTH), bioactive ACTH (bACTH), and ACTH-(1-39) in nine adrenalectomized fetuses at 126-130 and 136-140 days of gestation. Fetuses received 4 h of cortisol (2 micrograms.kg-1.min-1) or saline infusions on consecutive days. Blood was obtained before and at intervals during infusions. Arterial blood gases and hematocrits were normal and did not change with age. Plasma cortisol did not change during saline infusions but increased significantly (range 30-70 ng/ml) during cortisol infusions. Basal plasma iACTH, bACTH, ACTH-(1-39), and bACTH-to-iACTH and ACTH-(1-39)-to-iACTH ratios were significantly higher in the older fetuses. Cortisol infusions decreased plasma iACTH, bACTH, and ACTH-(1-39) in both groups, and the suppression as a percent of the baseline was similar. The bACTH-to-iACTH ratio declined to the same level at 126-130 (0.201 +/- 0.040 to 0.051 +/- 0.002) and 136-140 (0.389 +/- 0.088 to 0.046 +/- 0.002) days of gestation. These data suggest that physiological concentrations of cortisol selectively inhibit bACTH secretion, and the ACTH response to cortisol inhibition is not different between 126 and 140 days of gestation in adrenalectomized sheep fetuses.

Changes in glucocorticoid receptor mRNA in the developing ovine pituitary and the effects of exogenous cortisol

Developmental changes in pituitary glucocorticoid receptor (GR) mRNA were examined during gestation and early neonatal life using in situ hybridization. Pituitaries were harvested from sheep fetuses at days 60-80, 100-120, 130-135, 140-142 and term, and from lambs of days 0-7 and 30-60, and adults. GR mRNA was present in the pars distalis by day 60, levels increased through gestation, and there was a redistribution of GR mRNA, resulting in a relatively greater abundance at the base of the pars distalis. At term, there was a significant (P < 0.05 compared with the day 140-142 fetuses) elevation of GR mRNA, which was maintained in the newborn lamb, reaching highest levels at days 30-60 of neonatal life. GR mRNA was undetectable in the pars intermedia until day 120, but subsequently increased to high levels at term. Interestingly, the expression of GR mRNA in the pars intermedia dropped precipitously in the newborn (P < 0.05 compared with term), though levels recovered in the older lambs and adults. The regional and cellular distribution of GR mRNA correlated closely with the presence of immunoreactive GR (irGR) in the pituitary; the majority of irGR was present in the nuclei. Intrafetal infusion of cortisol (12 h; 5 micrograms/min) in late gestation (day 135) had no effect on Gr mRNA expression in either the pars distalis or pars intermedia.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of cortisol on the concentration of glycogen in different tissues in the chronically catheterized fetal pig.

The effect of exogenous cortisol on glycogen deposition in a number of fetal tissues was investigated in chronically catheterized fetal pigs between 80 and 95 d of gestation (term 114 d). Intravascular infusion of cortisol for 48 h increased the fetal plasma concentration of cortisol 4-fold to a value similar to that observed in piglets near to term. After infusion of cortisol, the concentration of glycogen in the lung was lower while the levels in skeletal muscle and liver were higher than those found in unoperated fetuses. There were no detectable changes in either skin or cardiac muscle glycogen after cortisol infusion. High endogenous cortisol concentrations were observed in some of the catheterized control fetuses and in two unoperated fetuses adjacent to the site of cortisol infusion. These fetuses also had detectable changes in lung, liver and skeletal muscle glycogen. When the data from all the fetuses, whether infused, control catheterized or unoperated, were combined there was a significant positive correlation between both liver and skeletal muscle glycogen concentrations and log plasma cortisol (r = 0.70 and 0.72 respectively, P less than 0.01). Lung glycogen levels were inversely related to log plasma cortisol (r = -0.67, P less than 0.01). No relation between either cardiac or skin glycogen concentration and fetal plasma cortisol could be detected. These observations demonstrate that cortisol has a marked effect on tissue glycogen levels in the immature fetal pig and suggest that the changes in glycogen concentrations observed in the liver, lung and skeletal muscle before term may be due to the pre-partum surge in fetal cortisol.