Showing papers on "Corticosterone published in 1983"
TL;DR: It is suggested that hippocampal [3H]corticosterone-binding sites and renal MR may have identical intrinsic specificity for steroids, with apparent specificity differences the result of tissue-specific sequestration of naturally occurring steroids other than Aldo.
Abstract: There is current evidence for two classes of hippocampal glucocorticoid receptors (GR)--one classical, [3H]dexamethasone [( 3H]Dex)-binding sites in glial cells, and the other [3H]corticosterone-preferring sites in neuronal cells. In the presence of 1 microM of the synthetic glucocorticoid RU26988 (11 beta, 17 beta-dihydroxy-17 alpha-propynylandrost-1,4,6,-trien-3-one) to exclude tracer from [3H]Dex sites, hippocampal cytosol from adrenalectomized/ovariectomized Sprague-Dawley rats binds [3H]Dex to sites (Kd at 4 degrees C, 0.77 X 10(-9) M; 65 fmol/mg of protein) with the following order of specificity: aldosterone (Aldo) = 9 alpha-fluorocortisol (9 alpha F-cortisol) = deoxycorticosterone (DOC) = corticosterone greater than cortisol much greater than Dex; [3H]Aldo, [3H]DOC, and [3H]corticosterone binding show identical specificity in the presence of RU26988. Addition of 1% adrenalectomized/ovariectomized rat plasma (but not plasma heated at 56 degrees C for 30 min) alters the specificity to: 9 alpha F-cortisol greater than or equal to Aldo greater than or equal to DOC much greater than Dex greater than or equal to corticosterone greater than or equal to cortisol, consistent with sequestration of DOC, corticosterone, and cortisol by transcortin and similar to classical mineralocorticoid receptor (MR) binding of [3H]Aldo in renal cytosol (9 alpha F-cortisol greater than or equal to Aldo greater than or equal to DOC much greater than corticosterone greater than or equal to cortisol greater than or equal to Dex). Separation of other renal binders from transcortin by hydroxylapatite adsorption established the intrinsic specificity of [3H]Aldo binding to MR as: DOC greater than or equal to Aldo greater than or equal to 9 alpha F-cortisol greater than or equal to corticosterone greater than cortisol much greater than Dex, parallel to that of the [3H]corticosterone-binding sites in hippocampus. These studies suggest (i) that hippocampal [3H]corticosterone-binding sites and renal MR may have identical intrinsic specificity for steroids, with apparent specificity differences the result of tissue-specific sequestration of naturally occurring steroids other than Aldo and (ii) that an identical steroid-binding species may thus be occupied under physiological conditions by a mineralocorticoid in one tissue (kidney) and a glucocorticoid in another (hippocampus).
519 citations
TL;DR: It is concluded that ketoconazole may be a general inhibitor of mitochondrial P450 enzymes, and the possibility that this drug action may be beneficially exploited in situations where inhibition of steroidogenesis is a therapeutic goal is raised.
Abstract: Ketoconazole has recently been shown to interfere with steroidogenesis in patients and rat in vitro systems. In this study we attempted to elucidate the site of inhibition in the adrenal gland. Although ketoconazole impaired adrenocorticotropic hormone stimulated cyclic (c)AMP production, dibutyrl cAMP addition did not bypass the steroidogenic blockade indicating that the critical ketoconazole-inhibited step was distal to cAMP. Addition of radiolabeled substrates to isolated adrenal cells and analysis of products by high performance liquid chromatography demonstrated a ketoconazole block between deoxycorticosterone (DOC) and corticosterone. This 11-hydroxylase step is carried out by a P450-dependent mitochondrial enzyme. No restriction of progesterone or pregnenolone conversion to DOC was detected, steps carried out by non-P450-dependent microsomal enzymes. Inhibition of cholesterol conversion to pregnenolone by mitochondrial fractions indicated a second block at the side chain cleavage step, another mitochondrial P450-dependent enzyme. Adrenal malate dehydrogenase, a non-P450-dependent mitochondrial enzyme was not inhibited while renal 24-hydroxylase, a P450-dependent mitochondrial enzyme in another organ, was blocked by ketoconazole. We conclude that ketoconazole may be a general inhibitor of mitochondrial P450 enzymes. This finding suggests that patients receiving ketoconazole be monitored for side effects relevant to P450 enzyme inhibition. Further, we raise the possibility that this drug action may be beneficially exploited in situations where inhibition of steroidogenesis is a therapeutic goal.
413 citations
TL;DR: Observations support the concept that there is an age-related loss of sensitivity of the brain and pituitary to the inhibitory effects of high circulating levels of corticosterone on ACTH release.
304 citations
TL;DR: It is indicated that glucocorticoids have a dual effect on type I collagen synthesis and alkaline phosphatase activity in cultured calvariae: a transient stimulatory effect after short term treatment and an inhibitory one after long term exposure.
Abstract: Glucocorticoid-induced osteoporosis is believed to be caused by increased bone resorption and decreased bone formation. However, the direct effects of glucocorticoids on bone formation are, as yet, not fully understood. Cortisol, corticosterone, and dexamethasone were examined for their effects on alkaline phosphatase activity, the incorporation of [3H]proline into type I collagen, DNA content, and mitotic index in intact 21-day-old fetal rat calvariae. After 24 h of treatment, cortisol at 1-100 nM increased the incorporation of [3H]proline into type I collagen, whereas at 1-10 microM, cortisol inhibited type I collagen labeling. After 96 h, cortisol (0.1-10 microM) had an inhibitory effect on type I collagen labeling and alkaline phosphatase activity. Cortisol had a small, not dose dependent, and transient stimulatory effect on alkaline phosphatase which appeared after 12-24 h of exposure, whereas the inhibitory effect was dose related, it appeared and was near-maximal after 48 h of continuous treatment with cortisol. Corticosterone and dexamethasone had an effect similar to that of cortisol on type I collagen synthesis and alkaline phosphatase activity. None of the steroids tested affected the release of the enzyme into the culture medium. Cortisol, corticosterone, and dexamethasone did not alter calvarial DNA content after 24 h of treatment, but after 96, concentrations of 1 nM to 10 microM were inhibitory. The decrease in DNA appeared after 48 h of exposure to 100 nM cortisol and was maximal after 72 h. Histological sections showed a marked and generalized decrease in the number of mitoses after colcemid arrest in calvariae treated with 100 nM cortisol, corticosterone, or dexamethasone for 96 h. These studies indicate that glucocorticoids have a dual effect on type I collagen synthesis and alkaline phosphatase activity in cultured calvariae: a transient stimulatory effect after short term treatment and an inhibitory one after long term exposure. The latter is related to a generalized decrease in cell population.
240 citations
TL;DR: Three potent stressors (forced running, immobilization, and footshock) were found to increase levels of cyclic AMP in the pituitaries of both female and male rats, and changes in plasma levels of prolactin, corticosterone, and growth hormone were unclear.
214 citations
TL;DR: It is concluded that the high affinity aldosterone receptor of rat brain, which had been identified in preliminary studies as a mineralocorticoid receptor, may bind either corticosterone or ald testosterone in vivo.
Abstract: The two [3H]aldosterone-binding proteins of rat brain cytosol were characterized by a dextran-coated charcoal method. With molybdate present to stabilize receptors, the affinities of the two sites for [3H]aldosterone in adrenalectomized perfused rat brain cytosols were 0.28 and 18.0 nM at 4 C. High affinity sites comprised 15% of the total receptor number. A small contamination of perfused brain cytosol preparations with corticosteroid-binding globulin (CBG) was found. However, due to the very high affinity of CBG for corticosterone at 4 C, this slight contamination resulted in significant alterations in the apparent affinity of steroids competing for aldosterone-binding sites. Selective precipitation of cytosol receptors with 36% (NH4)2SO4 reduced CBG concentrations to negligible levels. After blockade of low affinity sites with a highly selective glucocorticoid (RU 26988), the order of steroids in competing for the high affinity receptor was desoxycorticosterone greater than fludrocortisone greater than corticosterone greater than aldosterone greater than progesterone greater than dexamethasone. Readdition of a small quantity of dialyzed serum to cytosol preparations yielded a profile of steroid binding similar to that of the kidney mineralocorticoid receptor (aldosterone greater than desoxycorticosterone greater than corticosterone). The distribution of both receptors in brain regions of adrenalectomized rats was determined. Both receptors were at greatest density in the hippocampus and lowest density in the hypothalamus. The high affinity site was at greatest density in limbic regions, whereas the low affinity receptor, apparently identical to the glucocorticoid type II receptor, was at greatest density in cortex and cerebellum. It is concluded that the high affinity aldosterone receptor of rat brain, which had been identified in preliminary studies as a mineralocorticoid receptor, may bind either corticosterone or aldosterone in vivo.
196 citations
TL;DR: Significant declines were seen in hippocampus and amygdala quantitatively comparable to the decline observed in nuclear binding in these loci, which suggests that the primary deficit leading to nuclear depletion may be the reduction of cytosolic receptor number, rather than other possible factors such as the reduction in receptor affinity or translocation of steroid-receptor complex.
165 citations
TL;DR: It is concluded that NE is an excitatory hypothalamic monoamine for ACTH release in stress and that hypothalamic 5-HT activity is reduced after stress.
Abstract: Despite evidence that ACTH release after stress is under excitatory hypothalamic control, a stimulatory role for any of the monoamine neurotransmitters is yet to be clearly demonstrated. In the present investigation computerized gas chromatography/mass spectrometry was used to assess the neuronal activities of hypothalamic dopamine, norepinephrine (NE), and serotonin (5-HT) in rats after stress-induced ACTH release. Medial basal hypothalamic NE neuronal activity as assessed by the ratio of 3,4-dihydroxyphenylethyleneglycol (DHPG) to NE. (DHPG/NE) was elevated (P < 0.0005) within 2 min after a 3-min cold water swim stress. Ether stress also caused a marked elevation in NE activity (P < 0.0025). A highly significant positive correlation between the ratio of hypothalamic DHPG/NE and serum corticosterone was found over a large population of normal and stressed rats. Consistent with this relationship between hypothalamic NE neuronal activity and ACTH release being a causal one were the findings that 1) adrenal...
153 citations
TL;DR: In rats chronically exposed to the same stressor for 10 days immediately prior to the experiment, an attenuated pituitary cyclic AMP and plasma prolactin response was seen upon application of 15 min of that stressor on the day of the experiments, compared to the responses observed in the naive rats.
Abstract: The effects of five putative stressors (saline injection, cold exposure, forced running, immobilization, and footshock) on levels of pituitary cyclic AMP, plasma prolactin, corticosterone and growth hormone were examined. In naive rats exposed to 15 min of these stressors for the first time, running, immobilization and footshock increased levels of pituitary cyclic AMP, plasma corticosterone and prolactin and decreased growth hormone, typical of stress response in the rat. Cold exposure only increased corticosterone and saline injection did not affect any measured parameter. In rats chronically exposed to the same stressor (once a day for 15 min) for 10 days immediately prior to the experiment, an attenuated pituitary cyclic AMP and plasma prolactin response was seen upon application of 15 min of that stressor on the day of the experiment, compared to the responses observed in the naive rats.
131 citations
TL;DR: Low levels of receptors were found in the neuropil of the hippocampus, the lateral septum, the cortical nucleus of the amygdala and the entorhinal cortex, while all other brain regions had low levels of receptor.
114 citations
TL;DR: Results suggest that VIP contained in the chromaffin cells of the frog adrenal gland may exert a local action in stimulating corticosteroid production by the interrenal tissue.
TL;DR: The data indicate that neurochemical changes can be separated into changes due to the aversive nature of the stimulus and the ability to cope with a stressor and the inability to cope augments plasma catecholamine increases in response to a Stressor and prolongs their return to baseline values.
Abstract: Rats received 60 minutes of footshock that was escapable (coping group) or inescapable (noncoping group). Plasma taken by jugular catheter showed that noncoping rats, compared with coping rats, had significantly higher peak norepinephrine (NE) and epinephrine (E) concentrations and significantly longer elevation of these catecholamines after footshock. Similarly, plasma corticosterone levels remained elevated significantly longer after footshock in noncoping rats. In brain, hypothalamic NE concentrations were lower in noncoping rats compared with coping controls, and this difference remained for at least 30 minutes after shock. A fall in hippocampal NE concentration was seen only in coping rats once they learned to terminate shock. Our data indicate that neurochemical changes can be separated into changes due to the aversive nature of the stimulus and the ability to cope with a stressor. The inability to cope augments plasma catecholamine increases in response to a stressor and prolongs their return to baseline values. The latter is also true for corticosterone levels. The decrease in hippocampal NE in coping and the decrease in hypothalamic NE in noncoping rats is not due to footshock by itself but to the ability of the rat to terminate this stressor. No strong correlation between central and peripheral catecholamine changes became apparent except a possible negative correlation between hypothalamic NE and peripheral NE and E levels.
TL;DR: The results suggest that dexamethasone regulates its own receptor in placenta, and the physiological aspect of this phenomenon requires elucidation of the role of glucocorticoids on placental function in the rat.
Abstract: Binding of (3H)-dexamethasone was studied in high speed supernatant (HSS) of basal zone trophoblast and labyrinthine zone of rat placenta using an exchange assay. The system showed the following characteristics: (1) maximum binding was attained after 120 min of incubation; (2) molybdate was required in the medium to measure binding sites at 20 degrees C and equilibrium conditions; (3) exchange was near 90-100% between ligand and corticosterone added during a preincubation; (4) low capacity (190-250 fmoles/mg protein), high affinity (Kd 10(-8) M) binders were determined by saturation analysis; (5) competition with other steroids in vitro revealed that in basal zone trophoblast, only dexamethasone displaced the ligand, whereas in labyrinthine zone corticosterone, progesterone and testosterone competed to a smaller degree than dexamethasone. We have also studied the effect of in vivo treatment of pregnant rats for four days with dexamethasone, corticosterone, estradiol, progesterone or testosterone, on (3H)-dexamethasone binding. Of all tested compounds, only dexamethasone treatment (which was suspended 24 h before the experiment to prevent receptor occupancy by exogenous hormone) significantly decreased binding of the tritiated hormone in HSS of labyrinthine zone and basal zone trophoblast. These results suggest that dexamethasone regulates its own receptor in placenta. The physiological aspect of this phenomenon requires elucidation of the role of glucocorticoids on placental function in the rat.
TL;DR: It is concluded that corticosterone triggers a serotonin response and that the specificity of the cortic testosterone action suggests involvement of the steroid receptor system located postsynaptically to the raphe-hippocampal serotonin projection.
TL;DR: It is concluded that adrenal catecholamines play an important role in the modulation of consolidation of memory in rats subjected to adrenalectomy and the high circulating ACTH levels that follow long-term ADX may correct for the behaviorial deficit induced by the absence of adrenomedullectomy.
TL;DR: A more general involvement of the dopaminergic pathways of the NAS in schedule-induced behaviors and in concomitant plasma corticosterone changes is shown.
Abstract: In a series of four experiments the relationship between 6-OHDA lesions of the nucleus accumbens septum (NAS), schedule-induced behaviors and plasma corticosterone levels was explored. Data from the first experiment show a significant decrease in water intake during a scheduled food delivery test hour for 6-OHDA lesioned groups of rats compared with sham or non-lesioned groups of rats, while during the remaining 23 hours of the day water intake was the same for 6-OHDA lesioned and sham lesioned groups. In a second experiment similar decreases in schedule-induced wheelrunning were observed for 6-OHDA lesioned rats when compared with sham lesioned rats. Data from a third experiment showed significant increases in plasma corticosterone levels of rats in the presence of a scheduled food delivery compared with rats given non-scheduled food. In a fourth experiment it was shown that 6-OHDA lesions of the NAS abolish this increase of corticosterone levels in rats on a food delivery schedule. These data extend the findings of Robbins and Koob [19] and show a more general involvement of the dopaminergic pathways of the NAS in schedule-induced behaviors and in concomitant plasma corticosterone changes.
TL;DR: It is concluded that stress is not a major factor contributing to the massive effects of sleep deprivation on sleep parameters.
TL;DR: Angular methyl oxidation of cortisol to its 18-hydroxy and 18-oxoderivative in two hypertensive disorders is attributed to a derangement in adrenocortical functional zonation permitting access of glucocorticoid products into the mineraloc Corticoid-biosynthesizing system.
TL;DR: A permissive role for glucocorticoids in gastric mucosal protection induced by prostaglandin F2 beta, sulfhydryls, and cimetidine is suggested.
TL;DR: It is suggested that glucocorticoid stimulation of phosphatidylcholine synthesis in fetal lung is mediated by binding to specific receptors, with subsequent de novo synthesis of RNA and protein.
Abstract: To investigate further the mechanism whereby glucocorticoids accelerate the maturation of the pulmonary surfactant system, we studied both binding of glucocorticoids and their effect on phosphatidylcholine synthesis in organ cultures of fetal rabbit lung grown in serum-free medium. The greatest effect of dexamethasone (100 nM for 48 h) occurred at 24 days gestation when there was a 103% increase in the rate of choline incorporation into phosphatidylcholine and a 24% increase in the tissue content of disaturated phosphatidylcholine. Stimulation by corticosteroid was first observed after 12 h of exposure. Choline incorporation increased in a linear fashion for 36 h and then began to plateau; removal of the steroid after 24 h prevented any further increase in stimulation. The presence of other hormones in the culture medium was not a prerequisite for the corticosteroid action. Fetal sex had no influence on dexamethasone-induced phosphatidylcholine synthesis or on nuclear binding of dexamethasone. There was a...
TL;DR: It is concluded that CRF administered in a repeated or continuous manner to intact rats, while causing some pituitary desensitization, still elicits a significant degree of ACTH secretion despite the presence of elevated corticosterone release.
Abstract: We have examined the pattern of ACTH secretion in rats receiving two or more injections of synthetic ovine corticotropin-releasing factor (CRF). A first exposure of cannulated intact rats to CRF caused a blunting of the ACTH response when CRF was again injected 0.5-6 h later. Since plasma corticosterone levels stayed elevated for only 2 h after the first injection of CRF, the diminished pituitary responsiveness persisted at a time when plasma corticosterone levels had returned to control values. When cannulated adrenalectomized animals were subjected to a similar treatment, the blunting of the ACTH release due to the second injection of CRF, though present, was of significantly shorter duration. Duplication of the corticosterone levels that follow one CRF injection by exogenous administration of the steroid inhibited the subsequent ACTH response to CRF for a maximum of 2 h. Finally, CRF infused into intact rats for 14 days consistently caused elevation of both ACTH and corticosterone secretion. We conclude that CRF administered in a repeated or continuous manner to intact rats, while causing some pituitary desensitization, still elicits a significant degree of ACTH secretion despite the presence of elevated corticosterone release. This observation as well as the fact that CRF-injected adrenalectomized animals exhibit some blunting of their ACTH responses suggest that steroid feedback, while participating in the diminished ability of CRF to repeatedly stimulate ACTH release, does not represent the sole modulator of pituitary responsiveness.
TL;DR: Pituitary-adrenal responsiveness to stress induced by either psychological (novelty) or physiological stimuli was examined in young and old rats, finding no change with age in either sex in basal corticosterone levels or in the time course of the adrenocortical response.
TL;DR: Measurements of changes in muscle protein synthesis, insulin and corticosterone in vivo in refed food-deprived rats indicate that the acute increase in protein synthesis requires (a) insulin, (b) a fall in cortic testosterone, and (c) at least one other independent anabolic factor.
Abstract: Measurements of changes in muscle protein synthesis, insulin and corticosterone in vivo in refed food-deprived rats, some after pretreatment with anti-insulin serum or corticosterone, indicate that the acute increase in protein synthesis (20-40 min) requires (a) insulin, (b) a fall in corticosterone, since corticosterone acts at least in part by blocking insulin action, and (c) at least one other independent anabolic factor.
TL;DR: It is postulate that hormones from both adrenal medulla and cortex are involved in the retention of information post-stress, and that these hormones act directly on the CNS rather than via the pituitary, since the response to adrenalectomy is not dependent on the presence of the pituitsary gland.
TL;DR: Scatchard analysis revealed that 10(-6) M aldosterone and corticosterone increased the maximum binding capacity for T3 by 60 and 41%, respectively, and that the corticoids did not alter the value of the dissociation constant.
TL;DR: Restriction of body weight gain by allowing obese and lean mice food for only 4 h daily altered the pattern of corticosterone, but the values in the ob/ob mice remained higher than those in the lean mice.
Abstract: The present studies have examined the diurnal rhythm of corticosterone in genetically obese mice and in mice made obese by treatment with gold thioglucose. The values of corticosterone were significantly higher in the ob/ob mice than in lean mice at each of the four time points measured. The diurnal pattern for corticosterone in ob/ob mice, however, was similar to that in lean mice at both 6 and 12 weeks of age and had a nadir at 0700 h and a zenith at 1800 h. In mice with gold thioglucose-induced obesity, on the other hand, the corticosterone values were the same in the obese and lean control mice 6 weeks after treatment with gold thioglucose. By 12 weeks after gold thioglucose treatment, the obese animals had higher corticosterone levels in the morning than lean animals, but the peak values at 1800 h were not different. Restriction of body weight gain by allowing obese and lean mice food for only 4 h daily altered the pattern of corticosterone, but the values in the ob/ ob mice remained higher than thos...
Journal Article•
TL;DR: The results suggest that the effects observed in the NE-sensitive adenylate cyclase system after adrenalectomy are mediated by the loss of adrenal corticosteroids.
Abstract: Two weeks after bilateral adrenalectomy, the responsiveness of the norepinephrine (NE)-sensitive adenylate cyclase system in the rat frontal cortex was increased. This effect was restricted to the non-beta-component of the system as no change was observed in the cyclic AMP response elicited by isoproterenol after bilateral adrenalectomy, thus indicating that subpopulations of cortical NE receptor systems are under separate endocrine control. The effect of adrenalectomy on the NE-sensitive adenylate cyclase system could be completely reversed by administering corticosterone for 3 days. No changes in the cyclic AMP response to NE were observed 2 weeks after bilateral medullectomy. Furthermore, an increase in the responsiveness of the system was also observed 2 weeks after hypophysectomy. These results suggest that the effects observed in the NE-sensitive adenylate cyclase system after adrenalectomy are mediated by the loss of adrenal corticosteroids. Adrenalectomy did not alter the activities of either adenylate cyclase or phosphodiesterase. No apparent changes were observed in the maximum binding or dissociation constant values of either beta or alpha adrenoceptors as assessed with [3H]alprenolol, [3H]WB-4101 and [ [3H]clonidine. Furthermore, the effects of adrenalectomy cannot be accounted for by a shift in the diurnal variation of the system as the cyclic AMP response to NE in tissue from adrenalectomized animals was higher than that in tissue from shamoperated rats throughout a 24-hr period.
TL;DR: Chronic treatment of rats with a liquid diet containing ethanol resulted in the development of tolerance, and acute ethanol administration induced a significant rise in serum corticosterone levels which seemed to be related to blood ethanol concentration.
Abstract: Acute ethanol administration (2 g/kg IP) induced a significant rise in serum corticosterone levels which seemed to be related to blood ethanol concentration. Chronic ethanol administration, in the form of a liquid diet for 16 or 30 days, did not alter the levels of serum corticosterone. Chronic treatment of rats with a liquid diet containing ethanol resulted in the development of tolerance.
TL;DR: Pretreatment by 1-deaminopenicillamine, 2-(O-methyl)tyrosine arginine-vasopressin (dPTyr(Me)AVP), a potent antagonist of the vasopressor14,15, behavioural15 and ACTH-releasing properties of AVP, does not modify the ACTH and corticosterone secretion induced by exposure to a novel environment, but totally inhibits the increase of ACTH
Abstract: Most of the experimental evidence for a role of arginine-vasopressin (AVP) in adrenocorticotropic hormone (ACTH) release comes from in vitro studies. The multimolecular nature of the hypothalamic factor responsible for corticotropin (CRF) release has long been recognized, but the importance of AVP as a cofactor is controversial. The recently characterized 41-residue peptide fulfills the criteria for a physiological role in ACTH release and it is potentiated in vitro by AVP. In vivo, AVP is able to stimulate ACTH secretion, and Brattleboro rats, deficient in AVP, show a reduced activity of the hypothalamo-hypophysial-adrenocortical system (HHCS) (see ref. 13 for references). Direct evidence for involvement of AVP in the physiological release of ACTH is, however, still lacking. The recent development of AVP receptor antagonists provides the opportunity to test this hypothesis directly. I report here that pretreatment by 1-deaminopenicillamine, 2-(O-methyl)tyrosine arginine-vasopressin (dPTyr(Me)AVP), a potent antagonist of the vasopressor, behavioural and ACTH-releasing properties of AVP, does not modify the ACTH and corticosterone secretion induced by exposure to a novel environment, but totally inhibits the increase of ACTH and corticosterone levels induced by AVP. The results do not support the hypothesis for a physiological involvement of AVP in ACTH release.
TL;DR: In this paper, four-week-old chicks were fed on diets containing corticosterone (0, 5, 10, 20, and 40 mg/kg) for 9 days.