Journal articles on the topic 'Corticosterone'
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Cohen, Alia, Lia Savu, Roger Vranckx, Michelle Maya, and Emmanuel A. Nunez. "Effect of adrenalectomy at different pregnancy stages on maternal and fetal serum corticosteroid binding globulin and corticosterone in the rat." Acta Endocrinologica 122, no. 1 (January 1990): 121–26. http://dx.doi.org/10.1530/acta.0.1220121.
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Abstract The response of pregnant rat corticosteroid binding globulin to maternal adrenalectomy was studied as a function of the stage of pregnancy. Non-pregnant or pregnant rats were deprived of their adrenal glands during 4 days. In non-pregnant animals, adrenalectomy led to undetectable corticosterone levels and to the doubling of corticosteroid binding globulin. In pregnant rats adrenalectomized at 12 days and studied at 16 days, the serum corticosterone was likewise undetectable and the corticosteroid binding globulin was doubled as compared with pregnant rats of the corresponding age. In contrast, adrenalectomy from day 14 to 18 or from day 16 to 20 did not deplete the maternal serum corticosterone and the corticosteroid binding globulin remained unchanged. Under these conditions neither fetal corticosteroid binding globulin nor fetal corticosterone were modified. However, when the pregnant rats adrenalectomized from day 16 to 20 also received an injection of 30 mg of metyrapone on days 19 and 20 in order to inhibit fetal adrenal secretion, the maternal response was again a depletion of serum corticosterone together with an increase in corticosteroid binding globulin. Under these conditions, the fetus also reacted by a fall of corticosterone and a rise of corticosteroid binding globulin. Our results suggest that the maternal response of corticosteroid binding globulin to adrenalectomy depends on the pregnancy stage inasmuch as it may be influenced by a supply of corticosterone from the fetus during late pregnancy. Moreover, they show that in this late period, fetal corticosteroid binding globulin is regulated independently.
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Washburn, Brian E., Dana L. Morris, Joshua J. Millspaugh, John Faaborg, and John H. Schulz. "Using a Commercially Available Radioimmunoassay to Quantify Corticosterone in Avian Plasma." Condor 104, no. 3 (August 1, 2002): 558–63. http://dx.doi.org/10.1093/condor/104.3.558.
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AbstractUsing a commercially available corticosterone I125 double-antibody radioimmunoassay, we developed and validated an assay procedure for determining corticosterone levels in small-volume (≤30 μL) avian plasma samples. We evaluated this procedure's utility by measuring plasma corticosterone levels in Indigo Buntings (Passerina cyanea), American Goldfinches (Carduelis tristis), Red-eyed Vireos (Vireo olivaceus), and Mourning Doves (Zenaida macroura). Standard biochemical validations (e.g., parallelism, recovery of exogenous corticosterone) demonstrated that the assay accurately and precisely measured corticosterone in avian plasma. We used a stress capture protocol to physiologically validate the assay's ability to determine biologically important changes in corticosterone levels. Males and females from four bird species exhibited a significant increase in plasma corticosterone in response to capture, handling, and restraint. Baseline and stress-induced corticosterone levels in our study were similar to reported values for other passerine species using other radioimmunoassay procedures. Our results suggest that this radioimmunoassay procedure is very effective for determining corticosterone levels in small-volume avian plasma samples and is sensitive enough to detect biologically important changes in the adrenocortical activity of birds. Thus, this assay has considerable utility for measuring stress levels and stress responses in small birds (<15 g), from which only small volumes of plasma (≤30 μL) can be collected.Utilización de un Radioinmunoensayo Disponible Comercialmente para la Cuantificación de Corticosterona en el Plasma de AvesResumen. Desarrollamos y validamos un proceso de ensayo para determinar los niveles de corticosterona en muestras de pequeño volúmen (≤30 μL) de plasma de aves utilizando un radioinmunoensayo para corticosterona I125 de doble anticuerpo disponible comercialmente. Evaluamos este procedimiento midiendo los niveles de corticosterona en Passerina cyanea, Carduelis tristis, Vireo olivaceus y Zenaida macroura. Validaciones bioquímicas estándares (e.g., paralelismo, recuperación de corticoesteroide exógeno) demostraron que el ensayo midió de modo exacto y preciso la corticosterona en el plasma de las aves. Utilizamos un protocolo de captura que producía estrés para validar fisiológicamente la habilidad del ensayo de detectar cambios biológicamente importantes en los niveles de corticosterona. Hembras y machos de las cuatro especies de aves mostraron un incremento significativo en los niveles de corticosterona en el plasma en respuesta a la captura, manipulación y retención. Los niveles basales e inducidos por el estrés de nuestro estudio fueron similares a valores reportados para otras especies paserinas que utilizaron otros procedimientos de inmunoensayo. Nuestros resultados sugieren que este procedimiento de radioinmunoensayo es muy efectivo para determinar los niveles de corticosterona en muestras de pequeño volúmen de plasma de aves y que es suficientemente sensible como para detectar cambios biológicamente importantes en la actividad adenocortical de las aves. De esta manera, este ensayo presenta considerable utilidad para medir los niveles y respuesta al estrés en aves pequeñas (<15 g) de las cuales sólo es posible colectar pequeños volúmenes de plasma (≤30 μL).
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Goymann, Wolfgang, Erich Möstl, and Eberhard Gwinner. "Corticosterone Metabolites can be Measured Noninvasively in Excreta of European Stonechats (Saxicola torquata rubicola)." Auk 119, no. 4 (October 1, 2002): 1167–73. http://dx.doi.org/10.1093/auk/119.4.1167.
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Abstract Measurements of corticosterone levels from blood samples of birds provide accurate snapshots of systemic hormone concentrations. However, those birds must be caught and handled, which may be unfeasible especially when multiple sampling is required. Furthermore, handling causes stress and may therefore interfere with hormone measurements. Therefore a non-invasive technique was developed to measure metabolites of corticosterone in excreta of European Stonechats (Saxicola torquata rubicola) using a corticosterone enzyme-immunoassay. High-performance liquid chromatography of excreta of a female and a male stonechat injected with tritiated corticosterone showed that corticosterone is excreted in the form of numerous metabolites and that the corticosterone enzyme-immunoassay cross-reacted with most of those metabolites. Injection of adrenocorticotrophic hormone in one female and seven male stonechats led to a significant increase in the levels of excreted corticosteroid metabolites within 1 h 20 min after administration of adrenocorticotrophic hormone. These results suggest that the corticosterone enzyme-immunoassay used in this study provides a quantitative measure of excreted corticosteroid metabolite levels in European Stonechats and has the potential to replace plasma measurements of these hormones.
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Droste, Susanne K., Lotte de Groote, Helen C. Atkinson, Stafford L. Lightman, Johannes M. H. M. Reul, and Astrid C. E. Linthorst. "Corticosterone Levels in the Brain Show a Distinct Ultradian Rhythm but a Delayed Response to Forced Swim Stress." Endocrinology 149, no. 7 (March 20, 2008): 3244–53. http://dx.doi.org/10.1210/en.2008-0103.
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Circulating corticosterone levels show an ultradian rhythm resulting from the pulsatile release of glucocorticoid hormone by the adrenal cortex. Because the pattern of hormone availability to corticosteroid receptors is of functional significance, it is important to determine whether there is also a pulsatile pattern of corticosterone concentration within target tissues such as the brain. Furthermore, it is unclear whether measurements of plasma corticosterone levels accurately reflect corticosterone levels in the brain. Given that the hippocampus is a principal site of glucocorticoid action, we investigated in male rats hippocampal extracellular corticosterone concentrations under baseline and stress conditions using rapid-sampling in vivo microdialysis. We found that hippocampal extracellular corticosterone concentrations show a distinct circadian and ultradian rhythm. The PULSAR algorithm revealed that the pulse frequency of hippocampal corticosterone is 1.03 ± 0.07 pulses/h between 0900 and 1500 h and is significantly higher between 1500 and 2100 h (1.31 ± 0.05). The hippocampal corticosterone response to stress is stressor dependent but resumes a normal ultradian pattern rapidly after the termination of the stress response. Similar observations were made in the caudate putamen. Importantly, simultaneous measurements of plasma and hippocampal glucocorticoid levels showed that under stress conditions corticosterone in the brain peaks 20 min later than in plasma but clears concurrently, resulting in a smaller exposure of the brain to stress-induced hormone than would be predicted by plasma hormone concentrations. These data are the first to demonstrate that the ultradian rhythm of corticosterone is maintained over the blood-brain barrier and that tissue responses cannot be reliably predicted from the measurement of plasma corticosterone levels.
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Müller, Claudia, Bettina Almasi, Alexandre Roulin, Creagh W. Breuner, Susanne Jenni-Eiermann, and Lukas Jenni. "Effects of corticosterone pellets on baseline and stress-induced corticosterone and corticosteroid-binding-globulin." General and Comparative Endocrinology 160, no. 1 (January 2009): 59–66. http://dx.doi.org/10.1016/j.ygcen.2008.10.018.
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Hanafusa, Junko, Tomoatsu Mune, Tetsuya Tanahashi, Yukinori Isomura, Tetsuya Suwa, Mako Isaji, Hisashi Daido, Hiroyuki Morita, Masanori Murayama, and Keigo Yasuda. "Altered corticosteroid metabolism differentially affects pituitary corticotropin response." American Journal of Physiology-Endocrinology and Metabolism 282, no. 2 (February 1, 2002): E466—E473. http://dx.doi.org/10.1152/ajpendo.00065.2001.
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To evaluate the effects of altered corticosteroid metabolism on the hypothalamic-pituitary-adrenal axis, we examined rats treated with glycyrrhizic acid (G rats) or rifampicin (R rats) for 7 days. The half-life of exogenously administered hydrocortisone as a substitute for corticosterone was longer in G rats and shorter in R rats, with no differences in basal plasma levels of ACTH or corticosterone. The ACTH responses to human corticotropin-releasing factor (CRF) or insulin-induced hypoglycemia were greater in G rats and tended to be smaller in R rats compared with those in the control rats, whereas the corticosterone response was similar. No difference was observed in the content and mRNA level of hypothalamic CRF among the groups. The number and mRNA level of CRF receptor and type 1 11β-hydroxysteroid dehydrogenase (11-HSD1) mRNA level in the pituitary were increased in G rats but not changed in R rats, suggesting that chronically increased intrapituitary corticosterone upregulates pituitary CRF receptor expression. In contrast, CRF mRNA levels in the pituitary were increased in R rats. Our data indicate novel mechanisms of corticosteroid metabolic modulation and the involvement of pituitary 11-HSD1 and CRF in glucocorticoid feedback physiology.
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Romero, L. Michael, and Robin C. Romero. "Corticosterone Responses in Wild Birds: The Importance of Rapid Initial Sampling." Condor 104, no. 1 (February 1, 2002): 129–35. http://dx.doi.org/10.1093/condor/104.1.129.
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Abstract Corticosterone concentrations in birds usually rise in response to capture and handling, and it is often assumed that this change is predictable. We tested this assumption by leaving Gambel's White-crowned Sparrows (Zonotrichia leucophrys gambelii), House Sparrows (Passer domesticus), and Lapland Longspurs (Calcarius lapponicus) in nets or traps for 15 min following capture and comparing their corticosterone response over the next 60 min with birds removed immediately. White-crowned Sparrows and House Sparrows left in mist nets for 15 min and then bled had significantly elevated corticosterone concentrations compared to controls that were immediately removed from the net and bled. Corticosterone concentrations over the next 45 min of handling and restraint were similar between groups. In another experiment, White-crowned Sparrows and Lapland Longspurs were captured using seed-baited Potter traps. The corticosterone response of White-crowned Sparrows left in the trap for 15 min did not differ from White-crowned Sparrows removed immediately. Leaving Lapland Longspurs in the trap had no effect in the initial 10 min of handling and restraint, but at 30 and 60 min these birds had significantly lower corticosterone concentrations than longspurs removed immediately from the trap. These data indicate that failing to immediately remove birds from nets or traps can alter the corticosterone response to subsequent stressful stimuli in unpredictable ways. This result emphasizes that the elapsed time from capture is a critical variable in assessing stress responses in free-living birds. Respuestas de los Niveles de Corticosterona en Aves Silvestres: La Importancia de un Muestreo Inicial Inmediato Resumen. Las concentraciones de corticosterona en las aves usualmente aumentan en respuesta a la captura y manipulación, y muchas veces se supone que estos cambios son predecibles. Pusimos a prueba esta suposición reteniendo individuos de las especies Zonotrichia leucophrys gambelii, Passer domesticus y Calcarius lapponicus en redes o trampas durante los 15 minutos subsecuentes a la captura y comparamos sus respuestas en los niveles de corticosterona durante los siguientes 60 minutos con las de individuos removidos inmediatamente de las trampas y redes. Las muestras de sangre de Z. l. gambelii y P. domesticus que fueron obtenidas después de 15 minutos de retención en las redes tuvieron niveles de corticosterona significativamente más altos que las de los individuos control obtenidas inmediatamente después de la captura. Durante los 45 minutos siguientes de manipulación y captura, las concentraciones de corticosterona fueron similares entre los dos grupos. En otro experimento, Z. l. gambelii y C. lapponicus fueron capturados mediante trampas “Potter” cebadas con semillas. La respuesta en los niveles de corticosterona de Z. l. gambelii no fue diferente entre individuos retenidos en las trampas por 15 minutos e individuos removidos inmediatamente. Para individuos de C. lapponicus retenidos en las trampas no hubo un efecto durante los 10 minutos iniciales de manipulación y captura, pero a los 30 y 60 minutos estas aves tuvieron concentraciones significativamente menores que los individuos removidos inmediatamente. Estos resultados indican que al no remover inmediatamente a las aves de las redes o trampas, las respuestas en los niveles de corticosterona a estímulos estresantes pueden verse alteradas de una manera impredecible. Estos resultados enfatizan que en aves silvestres, el lapso de tiempo desde la captura es una variable crítica en la determinación de las respuestas al estrés.
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Remage-Healey, Luke, and L. Michael Romero. "Corticosterone and insulin interact to regulate glucose and triglyceride levels during stress in a bird." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 3 (September 1, 2001): R994—R1003. http://dx.doi.org/10.1152/ajpregu.2001.281.3.r994.
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Captive European starlings ( Sturnus vulgaris) were exposed to the stress of handling and restraint while corticosterone, glucose, and triglyceride concentrations were monitored in blood plasma. In saline-injected controls, basal samples were taken within 3 min of disturbance with subsequent samples taken at 40, 70, and 150 min. This was repeated at two times during the daily cycle (day and night) on two different photoperiods: short and long days. During both photoperiods, corticosterone concentrations approximately tripled (compared with a sixfold increase in free-living starlings) and triglyceride concentrations decreased 25–45% in response to stress at both times of the day, whereas an ∼25% stress-induced hyperglycemia occurred only at night. Exogenous corticosterone (200 μg), 1.0 or 4.0 IU/kg of insulin, or a combination of corticosterone with each insulin dose was then separately administered to alter the above responses. Insulin did not affect corticosterone or triglyceride concentrations but resulted in a dose-dependent hypoglycemia of 10–40%. Injected corticosterone resulted in supraphysiological corticosterone concentrations (three- to fivefold higher than normal), yet it did not affect the already altered plasma glucose or triglyceride concentrations. This suggests that glucose output and triglyceride decreases were already maximal in response to handling and restraint. However, the low glucose concentrations resulting from exogenous insulin returned to basal quicker with exogenous corticosterone but only during the day. No response to either hormone showed photoperiodic differences. These data suggest that corticosterone's role in metabolism changes to meet varying energetic demands throughout the day.
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Sheppard, K., and J. W. Funder. "Mineralocorticoid specificity of renal type I receptors: in vivo binding studies." American Journal of Physiology-Endocrinology and Metabolism 252, no. 2 (February 1, 1987): E224—E229. http://dx.doi.org/10.1152/ajpendo.1987.252.2.e224.
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We have injected rats with [3H]aldosterone or [3H]corticosterone, plus 100-fold excess of the highly specific glucocorticoid RU 28362, with or without excess unlabeled aldosterone or corticosterone and compared type I receptor occupancy in kidney and hippocampus. Thirty minutes after subcutaneous injection [3H]aldosterone was well retained in renal papilla-inner medulla, renal cortex-outer medulla, and hippocampus; in contrast, [3H]corticosterone was well retained only in hippocampus. Competition studies for [3H]aldosterone binding sites showed corticosterone to be a poor competitor in the kidney compared with hippocampus. Time-course studies, with rats killed 10-180 min after tracer administration, showed very low uptake/retention of [3H]corticosterone by kidney; in hippocampus [3H]corticosterone retention was similar to that of [3H]aldosterone in kidney, and retention of [3H]aldosterone by hippocampus was much more prolonged than of either tracer in any other tissue. Studies in 10-day-old rats, with very low levels of corticosteroid binding globulin (CBG), showed a high degree of aldosterone selectivity in both zones of the kidney, whereas [3H]aldosterone and [3H]corticosterone were equivalently bound in hippocampus. We interpret these data as evidence for a mechanism unrelated to extravascular CBG conferring mineralocorticoid specificity on renal type I receptors and propose two models derived from our findings consistent with such differential selectivity.
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Filaretova, L. P., A. A. Filaretov, and G. B. Makara. "Corticosterone increase inhibits stress-induced gastric erosions in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 6 (June 1, 1998): G1024—G1030. http://dx.doi.org/10.1152/ajpgi.1998.274.6.g1024.
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The role of glucocorticoids released in response to stress in the pathogenesis of stress-induced gastric erosions has been reevaluated. Gastric erosions elicited in male rats by 3-h cold-restraint or water-restraint stresses were studied after acute reduction of corticosterone release or occupation of glucocorticoid receptors by the antagonist RU-38486 during stress. Stress-induced corticosterone production was reduced by creating a lesion on the hypothalamic paraventricular nucleus (PVN) 4 days before stress as well as by pretreatment with a rabbit antiserum to adrenocorticotropin (ACTH) 30 min before stress. RU-38486 (10 mg/kg po) was administered 20 min before and 60 min after the onset of stress. Corticosterone for replacement was injected 15 min before the onset of stress to mimic stress-induced corticosterone response. Plasma corticosterone levels were measured by fluorometry or RIA. Gastric erosions were quantitated by measuring the area of damage. Four days after PVN lesion, stress-induced corticosterone release was decreased and gastric erosions were increased. Injecting corticosterone significantly attenuated the effect of PVN lesion on gastric erosions. The ACTH antiserum inhibited corticosteroid secretion in response to stress and markedly increased gastric erosions. The administration of the glucocorticoid/progesterone antagonist RU-38486 significantly potentiated the formation of stress-induced gastric erosions. These observations support the suggestion that glucocorticoids released during stress have a gastroprotective action rather than an ulcerogenic effect as was generally accepted.
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Bassett, J. R. "Enhanced corticosterone-binding capacity in plasma after stimulation of the rat adrenal cortex: the possibility of a simultaneous release of protein and corticosterone." Journal of Endocrinology 112, no. 1 (January 1987): 33–41. http://dx.doi.org/10.1677/joe.0.1120033.
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ABSTRACT Exposure of rats to either footshock or handling stress produced a significant increase in both plasma corticosterone concentration and specific binding capacity. Non-specific binding was eliminated using the synthetic glucocorticoid, dexamethasone. The increase in both plasma corticosterone and specific binding capacity was biphasic following exposure to footshock. Adrenalectomy and pretreatment with betamethasone abolished both phases of the enhanced binding capacity and plasma steroid concentration. Intraperitoneal injection of ACTH (1–24) in animals pretreated with betamethasone resulted in a biphasic rise in plasma concentrations of corticosterone but only the initial increase in binding capacity. Dissociation constant (Kd) values, determined by Scatchard analysis, for adrenalectomized and betamethasone-pretreated animals were 546 and 556 pmol/l respectively. These values were significantly different from the Kd in animals with functional adrenals (631 pmol/l). The results are discussed in the light of a possible specific corticosteroid-binding globulin (CBG)-like binding protein of adrenal origin released in conjunction with corticosterone. This binding protein has a lower affinity for corticosterone and a shorter half-life than CBG. J. Endocr. (1987) 112, 33–41
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Wotus, Cheryl, and William C. Engeland. "Differential regulation of adrenal corticosteroids after restriction-induced drinking in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 1 (January 1, 2003): R183—R191. http://dx.doi.org/10.1152/ajpregu.00027.2002.
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Water-restricted rats exhibit a rapid decrease in plasma corticosterone after drinking. The present study examined the effect of restriction-induced drinking on plasma aldosterone and plasma clearance of corticosterone. Rats were water restricted for 6–7 days and then killed before or 15 min after water administration; plasma and adrenal hormones were assayed. Plasma and adrenal corticosterone decreased after drinking without a change in plasma corticosteroid-binding globulin; plasma ACTH decreased or did not change. In contrast, plasma aldosterone did not change or increased after drinking; plasma renin activity was elevated by water restriction and increased further after drinking. In another experiment, rats were adrenalectomized, and corticosterone and aldosterone were replaced with pellets and osmotic minipumps, respectively. Rats were water restricted and killed. There was a small decrease in plasma corticosterone but no change in aldosterone after drinking in adrenalectomized animals. These data suggest that changes in plasma steroids after restriction-induced drinking result from zone-specific responses of the adrenal to known secretagogues, with minimal contribution from increased plasma clearance.
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van Gemert, Neeltje G., Diana M. M. Carvalho, Henk Karst, Siem van der Laan, Mingxu Zhang, Onno C. Meijer, Johannes W. Hell, and Marian Joëls. "Dissociation between Rat Hippocampal CA1 and Dentate Gyrus Cells in Their Response to Corticosterone: Effects on Calcium Channel Protein and Current." Endocrinology 150, no. 10 (July 9, 2009): 4615–24. http://dx.doi.org/10.1210/en.2009-0525.
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Abstract Stress and corticosterone affect, via glucocorticoid receptors, cellular physiology in the rodent brain. A well-documented example concerns corticosteroid effects on high-voltage activated (L type) calcium currents in the hippocampal CA1 area. We tested whether corticosterone also affects calcium currents in another hippocampal area that highly expresses glucocorticoid receptors, i.e. the dentate gyrus (DG). Remarkably, corticosterone (100 nm, given for 20 min, 1–4.5 hr before recording) did not change high-voltage activated calcium currents in the DG, whereas currents in the CA1 area of the same rats were increased. Follow-up studies revealed that no apparent dissociation between the two areas was observed with respect to transcriptional regulation of calcium channel subunits; thus, in both areas corticosterone increased mRNA levels of the calcium channel-β4 but not the (α) Cav1.2 subunit. At the protein level, however, β4 and Cav1.2 levels were significantly up-regulated by corticosterone in the CA1 but not the DG area. These data suggest that stress-induced elevations in the level of corticosterone result in a regionally differentiated physiological response that is not simply determined by the glucocorticoid receptor distribution and that the observed regional differentiation may be caused by a gene involved in the translational machinery or in mechanisms regulating mRNA or protein stability.
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Atkinson, Helen C., Susan A. Wood, Emma S. Castrique, Yvonne M. Kershaw, Crispin C. R. Wiles, and Stafford L. Lightman. "Corticosteroids mediate fast feedback of the rat hypothalamic-pituitary-adrenal axis via the mineralocorticoid receptor." American Journal of Physiology-Endocrinology and Metabolism 294, no. 6 (June 2008): E1011—E1022. http://dx.doi.org/10.1152/ajpendo.00721.2007.
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The aim of this study was to investigate fast corticosteroid feedback of the hypothalamic-pituitary-adrenal (HPA) axis under basal conditions, in particular the role of the mineralocorticoid receptor. Blood samples were collected every 5 min from conscious rats at the diurnal peak, using an automated blood sampling system, and assayed for corticosterone. Feedback inhibition by rapidly increasing concentrations of ligand was achieved with an intravenous bolus of exogenous corticosteroid. This resulted in a significant reduction in plasma corticosterone concentrations within 23 min of the aldosterone bolus and 28 min of methylprednisolone. Evaluation of the pulsatile secretion of corticosterone revealed that the secretory event in progress at the time of administration of exogenous steroid was unaffected, whereas the next secretory event was inhibited by both aldosterone and methylprednisolone. The inhibitory effect of aldosterone was limited in duration (1 secretory event only), whereas that of methylprednisolone persisted for 4–5 h. Intravenous administration of canrenoate (a mineralocorticoid receptor antagonist) also had rapid effects on the HPA axis, with an elevation of ACTH within 10 min and corticosterone within 20 min. The inhibitory effect of aldosterone was unaffected by pretreatment with the glucocorticoid receptor antagonist RU-38486 but blocked by the canrenoate. These data imply an important role for the mineralocorticoid receptor in fast feedback of basal HPA activity and suggest that mineralocorticoids can dynamically regulate basal corticosterone concentrations during the diurnal peak, a time of day when there is already a high level of occupancy of the cytoplasmic mineralocorticoid receptor.
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Sahin, A., and J. M. Forbes. "Diet selection in broiler chickens with corticosterone-induced changes in body composition." BSAP Occasional Publication 20 (1997): 121–23. http://dx.doi.org/10.1017/s0263967x00043603.
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Birds attempt to compensate for an E : P (energy: protein) imbalance by increasing their intake of protein or energy from selected foods and this is related to changes in the birds’ body composition caused by corticosterone treatment.Corticosterone injections increase fatness despite increasing nitrogen and energy excretion (Bartov, 1985). More recently corticosterone has been used to modulate macronutrient selection in rats (Devenport et al., 1991; Bligh et al., 1993; Tempel et al., 1993) and chickens (Covasa and Forbes, 1995). The intake of high protein concentrate was decreased by corticosterone treatment in young chickens but not in older chickens (Covasa and Forbes, 1995). The previous results suggest that more information on corticosterone’s effect on diet selection will be obtained by using foods which can offer a wide range of choices to compose a proper diet (Covasa and Forbes, 1995). Therefore, two experiments were conducted to detect changes in protein preference in relation to reduced protein deposition and enhanced fattening induced by corticosterone in male and female growing broiler chickens.
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Karst, Henk, and Marian Joëls. "Corticosterone Slowly Enhances Miniature Excitatory Postsynaptic Current Amplitude in Mice CA1 Hippocampal Cells." Journal of Neurophysiology 94, no. 5 (November 2005): 3479–86. http://dx.doi.org/10.1152/jn.00143.2005.
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Corticosteroid hormones are released in high amounts after stress and bind to intracellular receptors in the brain, which in activated form function as transcription factors. We here tested the effect of a high dose of corticosterone on AMPA-receptor–mediated transmission in the CA1 hippocampal area, which is enriched in corticosteroid receptors. To focus on slow gene-mediated effects of the hormone, excitatory postsynaptic currents were measured at least 1 h after a brief application of 100 nM corticosterone to slices from adrenally intact adult mice. The amplitude but not frequency of miniature postsynaptic excitatory currents was found to be significantly enhanced. These effects were mimicked by 100 nM RU 28362, a selective agonist for intracellular glucocorticoid receptors. Evoked AMPA responses at the single cell were significantly enhanced when measured 2–4 h after application of 100 nM corticosterone, but not at earlier moments nor with a longer delay. In summary, the present results show that activation of hippocampal glucocorticoid receptors induces a slow enhancement of AMPA-receptor–mediated responses, at the single-cell level.
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Silva, Ana M., Carina T. Ribeiro, Raquel L. Bernardino, Ivana Jarak, Rui A. Carvalho, M. A. Pereira-Sampaio, Diogo B. de Souza, Marco G. Alves, and Pedro F. Oliveira. "Stress Hormone Corticosterone Controls Metabolic Mitochondrial Performance and Inflammatory Signaling of In Vitro Cultured Sertoli Cells." Biomedicines 10, no. 9 (September 19, 2022): 2331. http://dx.doi.org/10.3390/biomedicines10092331.
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Stress, as a physiological response, is a major factor that affects several processes, including reproductive functions. The main hormonal players of stress are cortisol (humans) and corticosterone (rodents). Sertoli cells (SCs), as key contributors for the testicular homeostasis maintenance, are extensively challenged by different hormones, with glucocorticoid corticosterone being the signaling modulator that may impact these cells at different levels. We aimed to characterize how corticosterone modulates SCs energy balance, putting the mitochondrial performance and signaling output in perspective as the cells can disperse to the surroundings. TM4 mouse SCs were cultured in the absence and presence of corticosterone (in nM: 20, 200, and 2000). Cells were assessed for extracellular metabolic fluxes, mitochondrial performance (cell respirometry, mitochondrial potential, and mitochondrial complex expressions and activities), and the expression of androgen and corticosteroid receptors, as well as interleukine-6 (IL-6) and glutathione content. Corticosterone presented a biphasic impact on the extracellular fluxes of metabolites. Low sub-physiological corticosterone stimulated the glycolytic activity of SCs. Still, no alterations were perceived for lactate and alanine production. However, the lactate/alanine ratio was decreased in a dose-dependent mode, opposite to the mitochondrial complex II activity rise and concurrent with the decrease of IL-6 expression levels. Our results suggest that corticosterone finely tuned the energetic profile of mouse SCs, with sub-physiological concentrations promoting glycolytic expenditure, without translating into cell redox power and mitochondrial respiratory chain performance. Corticosterone deeply impacted the expression of the pro-inflammatory IL-6, which may alter cell-to-cell communication in the testis, in the last instance and impact of the spermatogenic performance.
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Waddell, B. J., and H. C. Atkinson. "Production rate, metabolic clearance rate and uterine extraction of corticosterone during rat pregnancy." Journal of Endocrinology 143, no. 1 (October 1994): 183–90. http://dx.doi.org/10.1677/joe.0.1430183.
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Abstract This study examined changes in the blood concentration of corticosterone with the onset and progression of pregnancy in the rat. To identify the source of variation in blood corticosterone, the metabolic clearance rate (MCR) and production rate of corticosterone were also determined. Measurements were made in conscious rats (n=4–7 per group) in the morning of dioestrus and days 5, 10, 16 and 22 of pregnancy (term=day 23). Corticosterone levels were 713 ±38 nmol/l (mean±s.e.m.) in non-pregnant rats, remained unchanged to day 10 of pregnancy, then increased to 1036 ± 52 nmol/l by day 16 and remained high at day 22. The production rate of corticosterone appeared to increase during pregnancy from 25·6±1·7 μmol/day on day 10 to reach 36·3±3·3 mol/day on day 22, but this did not reach statistical significance (one-way ANOVA). The MCR of corticosterone was similar among all groups (overall mean 34·6±2·5 1/day), although a slight but non-significant fall was apparent at day 16. When account was taken of changes in maternal weight, the MCR decreased progressively from 139± 10 1/day per kg before pregnancy to reach a minimum of 88 ±7 1/day per kg on day 16. Transuterine extraction of corticosterone on day 22 of pregnancy was 19·2±3·1% and so, based on this and estimates of uterine blood flow, the uterus must account for around 15% of corticosterone clearance at this time. Because this uterine contribution is effectively additional clearance, it is likely that without it the MCR of corticosterone would have fallen during pregnancy. Administration of ACTH (1–24) (3·5 nmol) increased the production rate of corticosterone at dioestrus and at day 16 of pregnancy, but this effect was less marked in the pregnant group (134% and 41% increase respectively). The MCR of corticosterone also rose (17%) following ACTH(1–24) administration in pregnant but not dioestrous rats. This difference in the MCR response is likely to reflect pregnancy-induced changes in the relative levels of corticosterone, progesterone and corticosteroid-binding globulin. In conclusion, this study shows that blood levels of corticosterone increase progressively during pregnancy in conscious rats. This increase apparently resulted from the net effects of increased production and decreased MCR, neither of which reached statistical significance. It would appear, however, that the trend toward increased production of corticosterone contributes more to the rise in blood corticosterone than does MCR, since the latter was more effectively maintained at pre-pregnancy levels. The demonstration of significant transuterine extraction of corticosterone at day 22 suggests that the maintenance of corticosterone clearance late in pregnancy is due, in part, to an additional contribution by the uterus and its contents. Journal of Endocrinology (1994) 143, 183–190
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Lowy, Martin T. "Corticosterone regulation of brain and lymphoid corticosteroid receptors." Journal of Steroid Biochemistry and Molecular Biology 39, no. 2 (August 1991): 147–54. http://dx.doi.org/10.1016/0960-0760(91)90055-a.
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Marissal-Arvy, Nathalie, Rachel Hamiani, Emmanuel Richard, Marie-Pierre Moisan, and Véronique Pallet. "Vitamin A regulates hypothalamic–pituitary–adrenal axis status in LOU/C rats." Journal of Endocrinology 219, no. 1 (July 11, 2013): 21–27. http://dx.doi.org/10.1530/joe-13-0062.
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The aim of this study was to explore the involvement of retinoids in the hypoactivity and hyporeactivity to stress of the hypothalamic–pituitary–adrenal (HPA) axis in LOU/C rats. We measured the effects of vitamin A deficiency administered or not with retinoic acid (RA) on plasma corticosterone in standard conditions and in response to restraint stress and on hypothalamic and hippocampal expression of corticosteroid receptors, corticotropin-releasing hormone and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in LOU/C rats. Interestingly, under control conditions, we measured a higher plasma concentration of retinol in LOU/C than in Wistar rats, which could contribute to the lower basal activity of the HPA axis in LOU/C rats. Vitamin A deficiency induced an increased HPA axis activity in LOU/C rats, normalized by RA administration. Compared with LOU/C control rats, vitamin A-deficient rats showed a delayed and heightened corticosterone response to restraint stress. The expression of corticosteroid receptors was strongly decreased by vitamin A deficiency in the hippocampus, which could contribute to a less efficient feedback by corticosterone on HPA axis tone. The expression of 11β-HSD1 was increased by vitamin A deficiency in the hypothalamus (+62.5%) as in the hippocampus (+104.7%), which could lead to a higher production of corticosterone locally and contribute to alteration of the hippocampus. RA supplementation treatment restored corticosterone concentrations and 11β-HSD1 expression to control levels. The high vitamin A status of LOU/C rats could contribute to their low HPA axis activity/reactivity and to a protective effect against 11β-HSD1-mediated deleterious action on cognitive performances during ageing.
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Gulfo, José, Joana Pérez de San Román, Angelo Ledda, Felix Junyent, María J. Ramírez, Francisco J. Gil-Bea, Montserrat Esteve, and Mar Grasa. "Corticosteroid-binding-globulin (CBG)-deficient mice show high pY216-GSK3β and phosphorylated-Tau levels in the hippocampus." PLOS ONE 16, no. 2 (February 16, 2021): e0246930. http://dx.doi.org/10.1371/journal.pone.0246930.
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Corticosteroid-binding globulin (CBG) is the specific carrier of circulating glucocorticoids, but evidence suggests that it also plays an active role in modulating tissue glucocorticoid activity. CBG polymorphisms affecting its expression or affinity for glucocorticoids are associated with chronic pain, chronic fatigue, headaches, depression, hypotension, and obesity with an altered hypothalamic pituitary adrenal axis. CBG has been localized in hippocampus of humans and rodents, a brain area where glucocorticoids have an important regulatory role. However, the specific CBG function in the hippocampus is yet to be established. The aim of this study was to investigate the effect of the absence of CBG on hippocampal glucocorticoid levels and determine whether pathways regulated by glucocorticoids would be altered. We used cbg-/- mice, which display low total-corticosterone and high free-corticosterone blood levels at the nadir of corticosterone secretion (morning) and at rest to evaluate the hippocampus for total- and free-corticosterone levels; 11β-hydroxysteroid dehydrogenase expression and activity; the expression of key proteins involved in glucocorticoid activity and insulin signaling; microtubule-associated protein tau phosphorylation, and neuronal and synaptic function markers. Our results revealed that at the nadir of corticosterone secretion in the resting state the cbg-/- mouse hippocampus exhibited slightly elevated levels of free-corticosterone, diminished FK506 binding protein 5 expression, increased corticosterone downstream effectors and altered MAPK and PI3K pathway with increased pY216-GSK3β and phosphorylated tau. Taken together, these results indicate that CBG deficiency triggers metabolic imbalance which could lead to damage and long-term neurological pathologies.
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Sarabdjitsingh, R. Angela, Sheena Isenia, Annelies Polman, Jona Mijalkovic, Servane Lachize, Nicole Datson, E. Ron de Kloet, and Onno C. Meijer. "Disrupted Corticosterone Pulsatile Patterns Attenuate Responsiveness to Glucocorticoid Signaling in Rat Brain." Endocrinology 151, no. 3 (January 15, 2010): 1177–86. http://dx.doi.org/10.1210/en.2009-1119.
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Chronically elevated circulating glucocorticoid levels are although to enhance vulnerability to psychopathology. Here we hypothesized that such sustained glucocorticoid levels, disturbing corticosterone pulsatility, attenuate glucocorticoid receptor signaling and target gene responsiveness to an acute challenge in the rat brain. Rats were implanted with vehicle or 40 or 100% corticosterone pellets known to flatten ultradian and circadian rhythmicity while maintaining daily average levels or mimic pathological conditions. Additionally, recovery from constant exposure was studied in groups that had the pellet removed 24 h prior to the challenge. Molecular markers for receptor responsiveness (receptor levels, nuclear translocation, promoter occupancy, and target gene expression) to an acute challenge mimicking the stress response (3 mg/kg ip) were studied in the hippocampal area. Implantation of 40 and 100% corticosterone pellets dose-dependently down-regulated glucocorticoid receptor and attenuated mineralocorticoid receptor and glucocorticoid receptor translocation to the acute challenge. Interestingly, whereas target gene Gilz expression to the challenge was already attenuated by tonic daily average levels (40%), Sgk-1 was affected only after constant high corticosterone exposure (100%), indicating altered receptor responsiveness due to treatment. Washout of 100% corticosterone recovered all molecular markers (partial), whereas removal of the 40% corticosterone pellet still attenuated responsiveness to the challenge. We propose that corticosteroid pulsatility is crucial in maintaining normal responsiveness to glucocorticoids. Whereas the results with 100% corticosterone are likely attributed to receptor saturation, subtle changes in the pattern of exposure (40%) induces changes at least as severe for glucocorticoid signaling as overt hypercorticism, suggesting an underlying mechanism sensitive to the pattern of hormone exposure.
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Pardridge, W. M., J. Eisenberg, G. Fierer, and R. W. Kuhn. "CBG does not restrict blood-brain barrier corticosterone transport in rabbits." American Journal of Physiology-Endocrinology and Metabolism 251, no. 2 (August 1, 1986): E204—E208. http://dx.doi.org/10.1152/ajpendo.1986.251.2.e204.
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The metabolic clearance rate of corticosterone in rabbits is unrelated to the physiological concentration of corticosteroid binding globulin (CBG) in rabbit plasma. This suggests that corticosterone is available for transport into peripheral tissues in rabbits from the circulating CBG-bound pool, similar to what is known to occur in rat liver. This hypothesis was tested in the present studies, which investigate the transport of corticosterone into rabbit brain from the circulating rabbit or human CBG-bound pool. Corticosterone was readily exchangeable in brain capillaries in vivo from the circulating albumin-bound and rabbit or human CBG-bound pools. The involvement of specific CBG receptors on brain capillary endothelia in this process was investigated with [3H]-labeled human CBG prepared by reductive methylation. The transport of [3H]CBG across rabbit brain capillaries in vivo was immeasurably low, and no specific binding of this radiolabeled plasma protein to isolated brain capillaries in vitro was observed at 37 degrees C during incubations up to 120 min. These studies indicate that the rabbit is a novel system for assessing the role of CBG in delivering corticosterone to peripheral tissues in vivo and that specific endothelial CBG receptors may not participate in the transport process.
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Moss, Emaya M., Fakhri Mahdi, Charlie J. Worth, and Jason J. Paris. "Physiological Corticosterone Attenuates gp120-Mediated Microglial Activation and Is Associated with Reduced Anxiety-Like Behavior in gp120-Expressing Mice." Viruses 15, no. 2 (February 2, 2023): 424. http://dx.doi.org/10.3390/v15020424.
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Despite the benefits of combinatorial antiretroviral therapies (cART), virotoxic HIV proteins are still detectable within the central nervous system. Approximately half of all cART-treated patients contend with neurological impairments. The mechanisms underlying these effects likely involve virotoxic HIV proteins, including glycoprotein 120 (gp120). Glycoprotein-120 is neurotoxic due to its capacity to activate microglia. Corticosterone has been found to attenuate neuronal death caused by gp120-induced microglial cytokine production in vitro. However, the concentration-dependent effects of corticosterone on microglial activation states and the associated behavioral outcomes are unclear. Herein, we conducted parallel in vitro and in vivo studies to assess gp120-mediated effects on microglial activation, motor function, anxiety- and depression-like behavior, and corticosterone’s capacity to attenuate these effects. We found that gp120 activated microglia in vitro, and corticosterone attenuated this effect at an optimal concentration of 100 nM. Transgenic mice expressing gp120 demonstrated greater anxiety-like behavior on an elevated plus maze, and a greater duration of gp120 exposure was associated with motor deficits and anxiety-like behavior. Circulating corticosterone was lower in gp120-expressing males and diestrous females. Greater circulating corticosterone was associated with reduced anxiety-like behavior. These findings may demonstrate a capacity for glucocorticoids to attenuate gp120-mediated neuroinflammation and anxiety-like behavior.
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Nedić, Sreten, Danijela Kirovski, Ivan Vujanac, Radiša Prodanović, Ljubomir Jovanović, Silvestra Kobal, and Tomaž Snoj. "Preventing ectoparasite infestations reduces glucocorticoid concentrations in the hair of cows – short communication." Acta Veterinaria Hungarica 66, no. 3 (September 2018): 390–93. http://dx.doi.org/10.1556/004.2018.035.
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The aim of this study was to compare hair corticosteroid concentrations in ectoparasiticide-treated (n = 10) and non-treated (n = 12) Holstein cows. Animals in the treated group received cyfluthrin three times, on days 0, 28 and 56 of the experiment. Hair samples were collected from all cows on days 0, 21, 42, 63, and 84 of the experiment for the determination of cortisol and corticosterone concentrations using immunoassays. The respective hair cortisol concentrations in the treated group averaged 209.78, 165.10, 260.78, 177.44 and 183.11 ng/g, while in the non-treated group hair cortisol concentrations averaged 172.58, 243.58, 309.73, 199.75 and 207.09 ng/g. These results indicate that the control of ectoparasites reduced hair cortisol levels in dairy cows. The respective hair corticosterone concentrations in the treated group averaged 19.06, 22.95, 21.95, 21.60 and 24.84 ng/g and in the non-treated group the hair corticosterone concentrations averaged 17.28, 21.94, 34.05, 26.27 and 26.91 ng/g. The results suggest that longterm stress can be estimated better by the determination of hair cortisol rather than corticosterone concentrations.
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Patterson-Buckendahl, P. E., R. E. Grindeland, D. C. Shakes, E. R. Morey-Holton, and C. E. Cann. "Circulating osteocalcin in rats is inversely responsive to changes in corticosterone." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 5 (May 1, 1988): R828—R833. http://dx.doi.org/10.1152/ajpregu.1988.254.5.r828.
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Decreased bone formation in rats during spaceflight may be attributable to corticosteroid excess induced by environmental factors other than weightlessness that are associated with spaceflight experiments. To determine whether decreased osteocalcin, which may reflect altered bone formation rate, could be associated with corticosteroid excess, we measured serum osteocalcin in rats after injection of corticosterone or in response to various environmental stimuli. Exogenous steroid elicited a time- and dose-related decrease in serum osteocalcin, which was significant within 1 h of administration and maximally 25% below controls 1.5 h after injection of 3.3 mg corticosterone/kg body wt, the highest dose we tested. Adrenalectomy resulted in a 38% increase in osteocalcin. Exposure to environmental stressors lasting from 1.5 h to 3 wk also resulted in decreased osteocalcin levels, which showed a strong negative correlation (P less than 0.001) with serum corticosterone levels and adrenal mass after 1-3 wk of chronic cold exposure. Changes in serum osteocalcin were maximally about +/- 40% after 3 wk of chronic exposure to steroid excess or depletion. The response of osteocalcin to the well-defined adrenal hormone system implies an important role for corticosteroids in the control of serum osteocalcin.
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Lynn, Sharon E., Thomas P. Hahn, and Creagh W. Breuner. "Free-Living Male Mountain White-Crowned Sparrows Exhibit Territorial Aggression Without Modulating Total or Free Plasma Testosterone." Condor 109, no. 1 (February 1, 2007): 173–80. http://dx.doi.org/10.1093/condor/109.1.173.
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Abstract Abstract In some species, expression of territorial aggression is accompanied by a rise in testosterone secretion, but in others aggressive behavior is expressed while testosterone levels remain unchanged. Corticosteroid binding globulin (CBG) binds both corticosterone and testosterone in avian plasma. Thus, increasing corticosterone may result in fluctuations in unbound (“free”) testosterone; this could result in greater biological activity of testosterone without an increase in testosterone secretion. We investigated whether such plasma interactions of testosterone, corticosterone, and CBG might result in alterations of free testosterone in male Mountain White-crowned Sparrows (Zonotrichia leucophrys oriantha). We conducted simulated territorial intrusions during incubation and compared total and free testosterone of males captured immediately following a simulated territorial intrusion with that of males captured passively. All experimental males showed aggressive behavior, but apparently did not modulate total or free testosterone relative to controls.
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Selyatitskaya, V. G., E. D. Afonnikova, N. A. Pal`chikova, and O. I. Kuz`minova. "Hypercorticism during streptozotocin diabetes and mifepristone administration: the role of cyclic adenosine monophosphate." Biomeditsinskaya Khimiya 65, no. 4 (2019): 311–15. http://dx.doi.org/10.18097/pbmc20196504311.
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It was studed basal and ACTH-stimulated production of cyclic adenosine monophosphate (cAMP) and corticosteroid hormones (progesterone and corticosterone) in rat adrenals in vitro under streptozotocin diabetes, in conditions of mifepristone administration and their combination. It was shown that in streptozotocin diabetes animals, both the basal and adrenocorticotropic hormone (ACTH) stimulated cAMP production significantly increased; this was accompanied by the increase in basal and ACTH-stimulated progesterone and corticosterone production in rat adrenals in vitro. Repeated administration of mifepristone to control and diabetic rats caused an increase mainly in ACTH-stimulated production of the main glucocorticoid hormone, corticosterone, without additional changes in the cAMP level. The results obtained suggest activation of two mechanisms of steroidogenesis enhancement in experimental animals. In rats with streptozotocin diabetes, both basal and ACTH-stimulated activity of all stages of steroidogenesis increase, which is mediated by the increased formation of cAMP as second messenger mediating the ACTH action on adrenocortical cells. Prolonged administration of mifepristone to control and diabetic rats resulted in increased activity of only late stages of steroidogenesis with predominant elevation of synthesis of physiologically active hormone corticosterone without additional changes in cAMP production level.
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Fässler, R., K. Schauenstein, G. Krömer, S. Schwarz, and G. Wick. "Elevation of corticosteroid-binding globulin in obese strain (OS) chickens: possible implications for the disturbed immunoregulation and the development of spontaneous autoimmune thyroiditis." Journal of Immunology 136, no. 10 (May 15, 1986): 3657–61. http://dx.doi.org/10.4049/jimmunol.136.10.3657.
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Abstract Basal plasma levels of corticosterone and corticosteroid-binding globulin (CBG) have been investigated in Obese strain (OS) chickens afflicted with spontaneous autoimmune thyroiditis (SAT). Corticosterone was determined radioimmunologically, and CBG by using a highly sensitive radioligand saturation assay. OS chickens displayed total corticosterone levels not different from healthy normal White Leghorn (NWL) chickens. CBG, however, was found to be twice as high in OS chickens as compared with their healthy counterparts, irrespective of sex or age. This quantitative difference in the CBG level is not compensated for by either altered affinity or specificity of the molecule. Furthermore, no differences were found in the response of OS and NWL lymphocytes to the suppressive effect of glucocorticoids in vitro. We therefore assume that OS animals are deficient in free, hormonally active corticosterone. An additional indication for such a diminished glucocorticoid tonus was that in vivo treatment of OS chickens with glucocorticoid hormones, thus increasing the free and active hormone fraction, normalizes the T cell hyperreactivity and significantly reduces thyroid infiltration. Possible pathophysiological implications of a diminished glucocorticoid tonus for spontaneous autoimmunity, as well as possible explanations for the beneficial effects of glucocorticoid treatment on the development of SAT, are discussed.
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Darlington, D. N., K. Kaship, L. C. Keil, and M. F. Dallman. "Vascular responsiveness in adrenalectomized rats with corticosterone replacement." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (May 1, 1989): H1274—H1281. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1274.
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To determine under resting, unstressed conditions the circulating glucocorticoid concentrations that best maintain sensitivity of the vascular smooth muscle and baroreceptor responses to vasoactive agents, rats with vascular cannulas were sham-adrenalectomized (sham) or adrenalectomized (ADRX) and provided with four levels of corticosterone replacement (approximately 100 mg fused pellets of corticosterone: cholesterol 0, 20, 40, and 80% implanted subcutaneously at the time of adrenal surgery). Changes in vascular and baroreflex responses were determined after intravenous injection of varying doses of phenylephrine and nitroglycerin with measurement of arterial blood pressure and heart rate in the conscious, chronically cannulated rats. Vascular sensitivity was decreased, and resting arterial blood pressure tended to be decreased in the adrenalectomized rats; both were restored to normal with levels of corticosterone (40%), which also maintained body weight gain, thymus weight, and plasma corticosteroid binding globulin concentrations at normal values. The baroreflex curve generated from the sham group was different from the curves generated from the ADRX+0, 20, and 40% groups, but not different from that of the ADRX+80% group, suggesting that the baroreflex is maintained by higher levels of corticosterone than are necessary for the maintenance of the other variables. These data demonstrate that physiological levels of corticosterone (40% pellet) restore vascular responsiveness, body weight, thymus weight, and transcortin levels to normal in ADRX rats, whereas higher levels (80% pellet) are necessary for restoration of the baroreflex.
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Rácz, K., J. Fehér, G. Csomós, I. Varga, R. Kiss, and E. Gláz. "An antioxidant drug, silibinin, modulates steroid secretion in human pathological adrenocortical cells." Journal of Endocrinology 124, no. 2 (February 1990): 341–45. http://dx.doi.org/10.1677/joe.0.1240341.
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ABSTRACT Because human adrenocortical cells from different adrenal disorders exhibit pathologically altered corticosteroid synthesis, and free radical mechanisms may induce pathological changes in the activities of corticosteroid biosynthetic enzymes (cytochrome P-450), we examined the effect of an antioxidant, silibinin, on basal and ACTH-stimulated secretion of several corticosteroids in isolated adrenal cells from an aldosterone-producing adenoma, atrophied adrenal tissues surrounding the adenoma, and hyperplastic adrenals from Cushing's syndrome. In the presence of a high concentration (100 μmol/l) of silibinin, variably diminished secretion of basal aldosterone, corticosterone, cortisol, 18-OH-corticosterone and 11-deoxycorticosterone was found. In contrast, the addition of 0·01 μmol silibinin/l, which failed to produce a clear effect on basal corticosteroid secretion, resulted in a potentiation of ACTH-stimulated secretion of several corticosteroids in the adenomatous and hyperplastic adrenocortical cells. These results suggest that the dose-dependent dual effect of silibinin on corticosteroid secretion may be attributed to corresponding changes in the activities of cytochrome P-450 enzymes, and that stimulation of ACTH-induced corticosteroidogenesis by silibinin is presumably due to the antioxidant property of the drug. Journal of Endocrinology (1990) 124, 341–345
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Karst, Henk, and Marian Joëls. "Effect of Chronic Stress on Synaptic Currents in Rat Hippocampal Dentate Gyrus Neurons." Journal of Neurophysiology 89, no. 1 (January 1, 2003): 625–33. http://dx.doi.org/10.1152/jn.00691.2002.
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We investigated the effect of chronic stress on synaptic responses of rat dentate granule cells to perforant path stimulation. Rats were subjected for 3 wk to unpredictable stressors twice daily or to control handling. One day after the last stressor, hippocampal slices were prepared and synaptic responses were determined with whole-cell recording. At that time, adrenal weight was found to be increased and thymus weight as well as gain in body weight were decreased in the stressed versus control animals, indicative of corticosterone hypersecretion during the stress period. In slices from rats with basal corticosteroid levels (at the circadian trough, under rest), no effect of prior stress exposure was observed on synaptic responses. However, synaptic responses of dentate granule cells from chronically stressed and control rats were differently affected by in vitro activation of glucocorticoid receptors, i.e., 1–4 h after administration of 100 nM corticosterone for 20 min. Thus the maximal response to synaptic activation of dentate cells at holding potential of −70 mV [when N-methyl-d-aspartate (NMDA) receptors are blocked by magnesium] was significantly enhanced after corticosterone administration in chronically stressed but not in control animals. In accordance, the amplitude of α-amino-3-hydroxy-5-methylisolazole-4-propionic acid (AMPA) but not of NMDA receptor-mediated currents was increased by corticosterone in stressed rats, over the entire voltage range. Corticosterone treatment also decreased the time to peak of AMPA currents, but this effect did not depend on prior stress exposure. The data indicate that following chronic stress exposure synaptic excitation of dentate granule cells may be enhanced when corticosterone levels rise. This enhanced synaptic flow could contribute to enhanced excitation of projection areas of the dentate gyrus, most notably the CA3 hippocampal region.
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Haeno, Satoko, Naoyuki Maeda, Takeshi Yagi, Sachi Tahata, Michiko Sato, Kanako Sakaguchi, Taku Miyasho, Hiromi Ueda, and Hiroshi Yokota. "Diethylstilbestrol decreased adrenal cholesterol and corticosterone in rats." Journal of Endocrinology 221, no. 2 (February 27, 2014): 261–72. http://dx.doi.org/10.1530/joe-13-0460.
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The synthetic oestrogen diethylstilbestrol (DES), which is known to bind oestrogen receptors (ERs), has been reported to have adverse effects on endocrine homeostasis; however, the molecular mechanisms underlying these effects are poorly understood. In this study, we treated rats with DES and found high levels of this compound in the liver, adrenal glands and pituitary gland, as compared with other tissues. We have also detected early adverse effects of DES in the adrenal glands. The adrenal glands of rats treated with DES (340 μg/kg body weight every 2 days) for 2 weeks showed increased weight and size and a decreased fat droplet size. Following 1 week of treatment with DES, the blood and adrenal corticosterone levels were substantially decreased without any histological alterations. The levels of the precursors for corticosteroid biosynthesis in the adrenal glands were also decreased, as determined using mass spectroscopy. Cholesterol, the principal material of corticosteroid biosynthesis, decreased substantially in the adrenal glands after only 1 week of treatment with DES. In conclusion, cholesterol insufficiency results in a reduction in adrenal corticosterone biosynthesis, which may lead to endocrine dysfunction, such as reproductive toxicity.
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Kern, Michael, Wayne Bacon, David Long, and Richard J. Cowie. "Blood Metabolite and Corticosterone Levels in Breeding Adult Pied Flycatchers." Condor 107, no. 3 (August 1, 2005): 665–77. http://dx.doi.org/10.1093/condor/107.3.665.
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AbstractWe describe how levels of glucose, triglyceride, fatty acids, glycerol, β-hydroxybutyrate, uric acid, and corticosterone varied in the blood of Pied Flycatchers (Ficedula hypoleuca) during three breeding cycles. Data are for egg-laying and incubating females, and adults of both sexes that were caring for nestlings. Egg-laying females had high blood levels of triglyceride, fatty acids, and uric acid. Triglyceride and fatty acids decreased steadily with the laying of each new egg, whereas uric acid increased. This pattern of change in blood lipids would be expected as the number of ovarian follicles that are loaded with yolk precursors and subsequently ovulated diminishes. The rising uric acid level probably reflects increased consumption and subsequent catabolism of dietary proteins. Corticosterone levels were low suggesting that food was readily available for the production of eggs. Incubating females used fat as fuel, most of which was probably of dietary origin given their low blood triglyceride coupled with high fatty acid, glycerol, and corticosterone levels, and stable, high body weight. None of the birds' plasma constituents varied with clutch size or the length of time the females had been incubating. Females rearing broods exhibited low triglyceride and high β-hydroxybutyrate and corticosterone levels. Blood glycerol and free fatty acids rose steadily as a function of nestling age, while glucose and body weight declined. Such a picture suggests that females underwent transient bouts of fasting while providing their chicks with food. Meanwhile males were lighter than their mates and had lower blood metabolite levels, but their blood corticosterone was elevated and correlated with uric acid levels, suggesting that they took more time to forage for themselves than females. Nonetheless, they too lost weight during this stage of the breeding cycle.Niveles Sanguíneos de Metabolitos y Corticosterona en Adultos Reproductivos de Ficedula hypoleucaResumen. Describimos la variación en los niveles sanguíneos de glucosa, triglicéridos, ácidos grasos, glicerol, betahidroxibutirato y corticosterona en Ficedula hypoleuca durante tres ciclos reproductivos. Los datos son para hembras que estaban poniendo o incubando huevos y para adultos de ambos sexos que estaban criando pichones. Las hembras que estaban poniendo huevos presentaron niveles altos de triglicéridos, ácidos grasos y ácido úrico. Los triglicéridos y ácidos grasos disminuyeron regularmente con la puesta de cada huevo nuevo, mientras que el ácido úrico aumentó. Este patrón de cambio en los lípidos sanguíneos era esperable debido a la disminución del número de folículos ováricos cargados con precursores de la yema que son subsecuentemente ovulados. El incremento en el nivel de ácido úrico probablemente refleja un incremento en el consumo y posterior catabolismo de proteínas dietarias. Los niveles de corticosterona fueron bajos, lo que sugiere que existía una alta disponibilidad de alimento para la producción de huevos. Las hembras que estaban incubando utilizaron las grasas como combustible. Considerando los niveles bajos de triglicéridos, los niveles altos de ácidos grasos, glicerol y corticosterona, y el peso corporal alto y estable de las aves, la mayor parte de estas grasas fue probablemente de origen dietario. Ninguno de los constituyentes del plasma sanguíneo varió con respecto al tamaño de la nidada o al período de tiempo durante el que las hembras habían estado incubando. Las hembras que estaban criando pichones presentaron niveles bajos de triglicéridos y niveles altos de betahidroxibutirato y corticosterona. El glicerol y los ácidos grasos sanguíneos se incrementaron con regularidad en función de la edad de los pichones, mientras que la glucosa y el tamaño corporal disminuyeron. Estos resultados sugieren que las hembras pasaron por períodos transitorios de ayuno mientras proveían alimento a sus pichones. Por su parte, los machos fueron más livianos que sus parejas y tuvieron niveles menores de metabolitos sanguíneos, pero su corticosterona sanguínea fue elevada y se corrrelacionó con los niveles de ácido úrico, lo que sugiere que los machos invirtieron más tiempo en forrajear para ellos mismos que las hembras. Sin embargo, los machos también perdieron peso durante esta etapa del ciclo reproductivo.
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Rose, James D. "Corticosteroid actions from neuronal membrane to behavior: Neurophysiological mechanisms underlying rapid behavioral effects of corticosterone." Biochemistry and Cell Biology 78, no. 3 (April 2, 2000): 307–15. http://dx.doi.org/10.1139/o00-021.
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Investigation of the rapid suppression of male courtship clasping behavior by corticosterone in roughskin newts (Taricha granulosa) has led to the identification of a specific neuronal membrane receptor for this stress steroid. This paper describes studies of the neurophysiological effects of the rapid, membrane receptor mediated action of corticosterone on neurons that are involved in the control of clasping. In freely behaving newts, medullary neurons, including reticulospinal neurons, process clasp-triggering sensory signals and participate in control of clasping movements. Corticosterone injection causes these brainstem neurons to show selective depression of clasping-related sensorimotor function. These corticosterone effects appear in 3-10 min and are closely associated with the simultaneous depression of clasping. In addition to these functionally specific effects, corticosterone simultaneously causes widespread, primarily depressive effects on neuronal activity and excitability in the medulla and elsewhere in the brain. Thus, the membrane actions of corticosterone lead to diverse neural effects, including changes in membrane excitability as well as specific, network-level actions that are apparent only during behavior. These rapid corticosterone effects strongly interact with actions of the neuropeptides vasotocin and corticotropin-releasing factor, such that the form and magnitude of the steroid's effects depend on the prevailing neuroendocrine state of the brain.Key words: glucocorticoid, membrane receptor, non-genomic, amphibian, reproduction.
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Yamaguchi, Tokutaro, Joo-Ho Lee, A.-Rang Lim, Joon-Soo Sim, Eun-Ji Yu, and Tae-Jin Oh. "Bioconversion of Corticosterone into Corticosterone-Glucoside by Glucosyltransferase." Molecules 23, no. 7 (July 19, 2018): 1783. http://dx.doi.org/10.3390/molecules23071783.
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Glucosylation of the 21-hydroxyl group of glucocorticoid changes its solubility into hydrophilicity from hydrophobicity and, as with glucocorticoid glucuronides as a moving object in vivo, it is conceivable that it exhibits the same behavior. Therefore, glucosylation to the 21-hydroxyl group while maintaining the 11β-hydroxyl group is particularly important, and glucosylation of corticosterone was confirmed by high-resolution mass spectrometry and 1D (1H and 13C) and 2D (COSY, ROESY, HSQC-DEPT and HMBC) NMR. Moreover, the difference in bioactivity between corticosterone and corticosterone 21-glucoside was investigated in vitro. Corticosterone 21-glucoside showed greater neuroprotective effects against H2O2-induced cell death and reactive oxygen species (ROS) compared with corticosterone. These results for the first time demonstrate that bioconversion of corticosterone through the region-selective glucosylation of a novel compound can present structural potential for developing new neuroprotective agents.
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Leckie, CM, and LA Welberg. "11beta-hydroxysteroid dehydrogenase is a predominant reductase in intact rat Leydig cells." Journal of Endocrinology 159, no. 2 (November 1, 1998): 233–38. http://dx.doi.org/10.1677/joe.0.1590233.
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11beta-Hydroxysteroid dehydrogenases (11beta-HSDs) interconvert active corticosterone and inert 11-dehydrocorticosterone. In tissue homogenates, 11beta-HSD type 1 (11beta-HSD-1) exhibits both 11beta-dehydrogenase (corticosterone inactivating) and 11beta-reductase (corticosterone regenerating) activities, whereas 11beta-HSD type 2 (11beta-HSD-2) is an exclusive dehydrogenase. In the rat testis, 11beta-HSD has been proposed to reduce glucocorticoid inhibition of testosterone production, promoting puberty and fertility. This hypothesis presupposes dehydrogenation predominates. 11beta-HSD-1 immunoreactivity has been localised to Leydig cells. However, recent studies suggest that 11beta-HSD-1 is predominantly an 11beta-reductase in many intact cells. We therefore examined the expression and reaction direction of 11beta-HSD isozymes in cultures of intact rat Leydig cells. Reverse transcriptase PCR demonstrated expression of 11beta-HSD-1, but not 11beta-HSD-2 mRNA in rat testis. Primary cultures of intact rat Leydig cells showed predominant 11beta-reductase activity, activating 50-70% of 11-dehydrocorticosterone to corticosterone over 3 h, whereas 11beta-dehydrogenation was <5%. Although both dexamethasone (10 nM) and corticosterone (1 microM) modestly inhibited LH-stimulated testosterone production by Leydig cells, inert 11-dehydrocorticosterone (1 microM) had similar effects, suggesting 11beta-reductase is functionally important. Carbenoxolone (10(-5) M) inhibited 11beta-reduction in intact Leydig cells. However, although carbenoxolone reduced Leydig cell testosterone production, this also occurred in the absence of glucocorticoids, suggesting effects distinct from modulation of corticosteroid access to Leydig cells. In conclusion, rat Leydig cell 11beta-HSD-1 is unlikely to reduce glucocorticoid access to testicular receptors. More likely, 11beta-reductase amplifies glucocorticoid action, perhaps to maintain Leydig cell metabolic and endocrine functions.
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Ivy, Jessica Ruth, Natalie K. Jones, Hannah M. Costello, Morag K. Mansley, Theresa S. Peltz, Peter W. Flatman, and Matthew A. Bailey. "Glucocorticoid receptor activation stimulates the sodium-chloride cotransporter and influences the diurnal rhythm of its phosphorylation." American Journal of Physiology-Renal Physiology 317, no. 6 (December 1, 2019): F1536—F1548. http://dx.doi.org/10.1152/ajprenal.00372.2019.
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The sodium-chloride cotransporter (NCC) in the distal convoluted tubule contributes importantly to sodium balance and blood pressure (BP) regulation. NCC phosphorylation determines transport activity and has a diurnal rhythm influenced by glucocorticoids. Disturbing this rhythm induces “nondipping” BP, an abnormality that increases cardiovascular risk. The receptor through which glucocorticoids regulate NCC is not known. In this study, we found that acute administration of corticosterone to male C57BL6 mice doubled NCC phosphorylation without affecting total NCC abundance in both adrenalectomized and adrenal-intact mice. Corticosterone also increased the whole kidney expression of canonical clock genes: period circadian protein homolog 1 ( Per1), Per2, cryptochrome 1, and aryl hydrocarbon receptor nuclear translocator-like protein 1. In adrenal-intact mice, chronic blockade of glucocorticoid receptor (GR) with RU486 did not change total NCC but prevented corticosterone-induced NCC phosphorylation and activation of clock genes. Blockade of mineralocorticoid receptor (MR) with spironolactone reduced the total pool of NCC but did not affect stimulation by corticosterone. The diurnal rhythm of NCC phosphorylation, measured at 6-h intervals, was blunted by chronic GR blockade, and a similar dampening of diurnal variation was seen in GR heterozygous null mice. These effects on NCC phosphorylation did not reflect altered rhythmicity of plasma corticosterone or serum and glucocorticoid-induced kinase 1 activity. Both mineralocorticoids and glucocorticoids emerge as regulators of NCC, acting via distinct receptor pathways. MR activation provides maintenance of the NCC protein pool; GR activation dynamically regulates NCC phosphorylation and establishes the diurnal rhythm of NCC activity. This study has implications for circadian BP homeostasis, particularly in individuals with abnormal glucocorticoid signaling as is found in chronic stress and corticosteroid therapy.
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Bossis, Ioannis, Shotaro Nishimura, Michael Muchow, and Tom E. Porter. "Pituitary Expression of Type I and Type II Glucocorticoid Receptors during Chicken Embryonic Development and Their Involvement in Growth Hormone Cell Differentiation." Endocrinology 145, no. 7 (July 1, 2004): 3523–31. http://dx.doi.org/10.1210/en.2004-0155.
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Abstract Glucocorticoids can induce somatotroph differentiation in vitro and in vivo during chick embryonic and rat fetal development. In the present study, we identified the nuclear receptors involved in somatotroph differentiation and examined their ontogeny and cellular distribution during pituitary development in the chicken embryo. Several steroids were tested for their ability to induce GH cell differentiation. Only glucocorticoids and aldosterone were effective at low nanomolar concentrations, suggesting involvement of both type I (mineralocorticoid) and type II (glucocorticoid) receptors (MR and GR, respectively). ZK98299 and spironolactone (GR and MR antagonists, respectively) when used alone were unable to block corticosterone or aldosterone (2 nm)-induced somatotroph differentiation. However, ZK98299 and spironolactone in combination abolished corticosterone or aldosterone (2 nm)-induced somatotroph differentiation. When used separately, both antagonists attenuated induction of GH mRNA by corticosterone. Spironolactone alone blocked somatotroph differentiation induced by 0.2 nm corticosterone or aldosterone, indicating that corticosteroids at subnanomolar concentrations act only through the MR. GR protein was detected in pituitary extracts as early as embryonic d 8, whereas MR protein was readily detectable only around d 12. GR were expressed in greater than 95% of all pituitary cells, whereas MR were expressed in about 40% of all pituitary cells. Dual-label immunofluorescence revealed that the majority of somatotrophs on d 12 expressed MR. Given the high affinity of corticosteroids for MR and that corticosteroid concentrations during embryonic development are in the subnanomolar range, expression of MR may constitute a significant developmental event during somatotroph differentiation.
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Petersen, Helle Heibroch, Thomas K. Andreassen, Tilman Breiderhoff, Jan Hinrich Bräsen, Herbert Schulz, Volkmar Gross, Hermann-Josef Gröne, Anders Nykjaer, and Thomas E. Willnow. "Hyporesponsiveness to Glucocorticoids in Mice Genetically Deficient for the Corticosteroid Binding Globulin." Molecular and Cellular Biology 26, no. 19 (October 1, 2006): 7236–45. http://dx.doi.org/10.1128/mcb.00400-06.
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ABSTRACT Corticosteroid binding globulin (CBG) is the carrier for glucocorticoids in plasma. The protein is believed to keep the steroids inactive and to regulate the amount of free hormone acting on target tissues (free hormone hypothesis). Here, we generated a mouse model genetically deficient for CBG to test the contribution of the carrier to glucocorticoid action and adrenocortical stress response. The absence of CBG resulted in a lack of corticosterone binding activity in serum and in an ∼10-fold increase in free corticosterone levels in CBG-null mice, consistent with its role in regulation of circulating free hormone levels. Surprisingly, cbg − / − animals did not exhibit features seen in organisms with enhanced glucocorticoid signaling. Rather, the mice exhibited increased activity of the pituitary axis of hormonal control, normal levels of gluconeogenetic enzymes, and fatigue, as well as an aggravated response to septic shock, indicating an inability to appropriately respond to the excess free corticosterone in the absence of CBG. Thus, our data suggest an active role for CBG in bioavailability, local delivery, and/or cellular signal transduction of glucocorticoids that extends beyond a function as a mere cargo transporter.
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Bradbury, Margaret J., William C. Dement, and Dale M. Edgar. "Effects of adrenalectomy and subsequent corticosterone replacement on rat sleep state and EEG power spectra." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 2 (August 1, 1998): R555—R565. http://dx.doi.org/10.1152/ajpregu.1998.275.2.r555.
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Individual effects of corticotropin-releasing hormone (CRH) and glucocorticoids on sleep have been difficult to discern due to the feedback effects each hormone exerts on the other. In addition, it is not known whether hypothalamic-pituitary-adrenal axis hormones alter sleep homeostasis or circadian influences on sleep propensity. We therefore analyzed sleep architecture and electroencephalographic (EEG) power in freely moving rats before and after removal of corticosterone (thus elevating endogenous CRH) by surgical adrenalectomy. Adrenalectomy reduced the amplitude of the diurnal rhythms of maximal and average sleep bout lengths ( P < 0.004). After adrenalectomy, power from 1 to 4 Hz decreased ( P < 0.042), whereas power from 9 to 12 Hz increased in the power spectra of the EEG recording ( P = 0.001). Administration of physiological corticosterone replacement reversed some of these effects. Supraphysiological corticosterone replacement in adrenalectomized rats reduced the amount of non-rapid-eye-movement sleep in the 24-h cycle ( P = 0.001). During each endocrine condition, rats were sleep deprived for 6 h. Endocrine status did not alter the subsequent homeostatic response to sleep deprivation. Thus ADX and supraphysiological corticosteroid replacement each altered sleep architecture without a demonstrable effect on sleep homeostasis.
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Bayburina, G. A. "Features of the dynamics of corticosteroid receptors in the myocardium of animals with different resistance to hypoxia in the post resuscitation period." Kazan medical journal 101, no. 1 (February 11, 2020): 40–46. http://dx.doi.org/10.17816/kmj2020-40.
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Aim. To characterize the peculiarities of the dynamics of the level of corticosteroid receptors in the myocardium of animals with different resistance to hypoxia in the post-resuscitation period.
Methods. Experimental studies were carried out on male non-inbred white rats, divided into 2 groups by hypoxia resistance. A 5-minute arrest of the systemic circulation was modeled under ether anesthesia with intrathoracic clamping of the cardiovascular cluster with subsequent resuscitation. The observation period was 35 days. The content of corticosterone and aldosterone was determined in the blood plasma, the concentration of glucocorticoid and mineralocorticoid receptors in myocard homogenates was determined as well.
Results. On days 1 to 3 of the post-resuscitation period in rats highly resistant to hypoxia, the dynamics of plasma corticosterone concentration and the content of corticosteroid receptors was unidirectional. Starting from the 5th day, against the background of a statistically significant decrease in the level of plasma corticosterone, a gradual increase in the density of corticosteroid receptors, mostly glucocorticoid, was observed, most pronounced on the 14th day and remaining until the end of the observation. In animals with low resistance to hypoxia, the dynamics of corticosteroid receptors was characterized by a predominance of mineralocorticoid content in almost all periods of observation. On days 13 of post-resuscitation period on the background of high concentrations of corticosteroid hormones, the minimum content of glucocorticoid receptors was noted. A decrease in the mineralocorticoid receptor level was recorded only on the first day, and in all subsequent periods of the experiment, the control indicators were significantly higher by 1.41.6 times. Strengthened mineralocorticoid signaling in the myocardium, characteristic of animals with low resistance to hypoxia, may be associated with the development of hypertrophy and fibrosis, inflammation, impaired electrical function. An increase in glucocorticoid receptors, characteristic of animals with a high resistance to hypoxia, has an adaptive effect, limiting the inflammatory response, the potential mechanism may be associated with increased expression of type 11-hydroxysteroid dehydrogenase.
Conclusion. The identified features can have a significant influence on the course of the post-resuscitation period and determine the long-term forecast.
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Duncan, R. L., W. M. Grogan, L. B. Kramer, and C. O. Watlington. "Corticosterone's metabolite is an agonist for Na+ transport stimulation in A6 cells." American Journal of Physiology-Renal Physiology 255, no. 4 (October 1, 1988): F736—F748. http://dx.doi.org/10.1152/ajprenal.1988.255.4.f736.
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This study tests the hypothesis, in A6 epithelia, that 1) corticosterone stimulates active Na+ transport (short-circuit current, Isc) by an additional receptor mechanism to the type I (mineralocorticoid) and type II (glucocorticoid) mechanisms shared with aldosterone (Aldo) and 2) that the agonist may be 6 beta-OH-corticosterone made in the effector cell. The dose-response relationship of corticosterone at 24 h resolves into two components, by curve fitting, with a 50% effective concentration (EC50) for 10% of maximum Isc stimulation of 2 X 10(-9) M and an EC50 for the other 90% of 3 X 10(-7) M. The EC50 of the smaller component correlates with the apparent dissociation constant (K'd) of corticosterone for high affinity (type II) nuclear binding sites shared with Aldo. In unlabeled analogue competition studies Aldo and corticosterone displaced nuclear binding equally below 10(-8) M [3H]corticosterone, indicating only shared sites. However, nonshared saturable sites (displaced by corticosterone but not by Aldo) were found at [3H]-corticosterone concentrations above 10(-8) M. Concentration-binding curves performed with [3H]corticosterone, in presence of 1,000 X Aldo to displace shared sites, revealed a single class of binding sites with a half-maximal saturation of 2 X 10(-7) M, which is quite similar to the EC50 of the lower affinity component of Isc stimulation by corticosterone at 24 h. Reversed phase high-pressure liquid chromatography of nuclear extracts indicates that the saturable component of bound [3H] was 6 beta-OH-[3H]corticosterone derived from [3H]corticosterone. Thus, A6 cells metabolize corticosterone to 6 beta-OH-corticosterone, which in turn occupies lower-affinity receptors not shared with Aldo or corticosterone, to mediate most of the active Na+ transport stimulation by corticosterone.
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Ludders, JW, JA Langenberg, NM Czekala, and HN Erb. "Fecal corticosterone refects serum corticosterone in Florida Sandhill Cranes." Veterinary Anaesthesia and Analgesia 27, no. 2 (July 2000): 111. http://dx.doi.org/10.1016/s1467-2987(16)31369-1.
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Ludders, John W., Julie A. Langenberg, Nancy M. Czekala, and Hollis N. Erb. "Fecal Corticosterone Reflects Serum Corticosterone in Florida Sandhill Cranes." Journal of Wildlife Diseases 37, no. 3 (July 2001): 646–52. http://dx.doi.org/10.7589/0090-3558-37.3.646.
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Whitehouse, B. J., S. J. Purdy, and D. R. E. Abayasekara. "Inhibition of corticosteroid production by sodium pentobarbitone in rat adrenocortical preparations." Journal of Endocrinology 136, no. 1 (January 1993): 75–83. http://dx.doi.org/10.1677/joe.0.1360075.
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ABSTRACT It is possible that some of the effects of sodium pentobarbitone on the hypothalamo-pituitary-adrenal axis in the intact animal may be attributable to direct actions on the adrenal cortex. The effects of the barbiturate on steroid production by rat adrenal preparations in vitro have therefore been examined. In zona glomerulosa cells, pentobarbitone inhibited basal steroid production in a dose-related fashion. For aldosterone and corticosterone, the doses required for 50% inhibition of production (IC50) were 1·2 mmol pentobarbitone/l and 3·7 mmol/l respectively. Steroidogenesis was inhibited at lower levels of pentobarbitone in the presence of 1 nmol ACTH/l (IC50 = 0·5 mmol pentobarbitone/l for aldosterone and 2·2 mmol/l for corticosterone). In zona fasciculata/reticularis cells, production of corticosterone was similarly reduced with an IC50 of 2·8 mmol pentobarbitone/l for basal production and 1·3 mmol/l for ACTH-stimulated production. The dose-related increases in corticosterone production produced by ACTH (0·1–1000 pmol/l) or dibutyryl cyclic AMP (0·1–1·0 mmol/l) were also eliminated in the presence of 2 mmol pentobarbitone/l. The effects of pentobarbitone (1–4 mmol/l) on the production of pregnenolone and deoxycorticosterone (DOC) were also studied. In zona fasciculata/reticularis cells, the responses of both pregnenolone and DOC were bell-shaped with increases at 1 mmol pentobarbitone/l, which fell back to control levels at 4 mmol pentobarbitone/l. Stimulation of DOC, accompanied by decreases in aldosterone and corticosterone production, was also seen in zona glomerulosa cells at 1 mmol pentobarbitone/l. The effect of 1 mmol pentobarbitone/l on the conversion of 22(R)-hydroxycholesterol (5-cholestene-3β,22(R)-diol), pregnenolone, progesterone and DOC to corticosterone and aldosterone by zona glomerulosa preparations was studied. There was a comparable reduction in the conversion of these precursors (2 μmol/l) to aldosterone with yields decreased to 20–30% of those found in the absence of pentobarbitone. The dose required for 50% reduction of the conversion of progesterone (2 μmol/l) to aldosterone was 0·55 mmol pentobarbitone/l and for corticosterone the dose was 1·75 mmol pentobarbitone/l. The results obtained show that pentobarbitone is an effective inhibitor of corticosteroid biosynthesis in rat adrenal cells, and suggest that its effects are brought about by inhibition of cytochrome P450-mediated hydroxylations. Journal of Endocrinology (1993) 136, 75–83
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Strack, A. M., M. J. Bradbury, and M. F. Dallman. "Corticosterone decreases nonshivering thermogenesis and increases lipid storage in brown adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 1 (January 1, 1995): R183—R191. http://dx.doi.org/10.1152/ajpregu.1995.268.1.r183.
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Brown adipose tissue (BAT) contains glucocorticoid receptors; glucocorticoids are required for maintaining differentiated BAT in culture. These studies were performed to determine the effects of corticosterone on BAT thermogenic function and lipid storage. Rats were adrenalectomized and given subcutaneous corticosterone pellets in concentrations that maintained plasma corticosterone constant across the range of 0-20 micrograms/dl or were sham adrenalectomized. All variables were examined 5 days after surgery and corticosterone replacement. Measures of BAT function-thermogenic capacity [guanosine 5'-diphosphate (GDP) binding and uncoupling protein (UCP; a BAT-specific thermogenic protein)] and storage (BAT wet wt, protein, and DNA levels) were made. Plasma hormones (corticosterone, adrenocorticotropic hormone, insulin, 3,3',5-triiodothyronine, and thyroxine were measured. Corticosterone significantly affected BAT thermogenic measures: UCP content and binding of GDP to BAT mitochondria decreased with increasing corticosterone; GDP binding characteristics in BAT from similarly prepared rats examined by Scatchard analysis showed that maximum binding (Bmax) and dissociation constant (Kd) decreased with increasing corticosterone dose. BAT DNA was increased by adrenalectomy and maintained at intact levels with all doses of corticosterone; BAT lipid storage increased dramatically at corticosterone values higher than the daily mean level in intact rats. Histologically, the number and size of lipid droplets within BAT adipocytes increased markedly with increased corticosterone. White adipose depots were more sensitive to circulating corticosterone concentrations than were BAT depots and increased in weight at levels of corticosterone that were at or below the daily mean level of intact rats. We conclude that, within its diurnal range of concentration corticosterone acts to inhibit nonshivering thermogenesis and increase lipid storage.(ABSTRACT TRUNCATED AT 250 WORDS)
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Richard, Elodie M., Jean-Christophe Helbling, Claudine Tridon, Aline Desmedt, Amandine M. Minni, Martine Cador, Line Pourtau, Jan-Pieter Konsman, Pierre Mormède, and Marie-Pierre Moisan. "Plasma Transcortin Influences Endocrine and Behavioral Stress Responses in Mice." Endocrinology 151, no. 2 (February 1, 2010): 649–59. http://dx.doi.org/10.1210/en.2009-0862.
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Glucocorticoids are released after hypothalamus-pituitary-adrenal axis stimulation by stress and act both in the periphery and in the brain to bring about adaptive responses that are essential for life. Dysregulation of the stress response can precipitate psychiatric diseases, in particular depression. Recent genetic studies have suggested that the glucocorticoid carrier transcortin, also called corticosteroid-binding globulin (CBG), may have an important role in stress response. We have investigated the effect of partial or total transcortin deficiency using transcortin knockout mice on hypothalamus-pituitary-adrenal axis functioning and regulation as well as on behaviors linked to anxiety and depression traits in animals. We show that CBG deficiency in mice results in markedly reduced total circulating corticosterone at rest and in response to stress. Interestingly, free corticosterone concentrations are normal at rest but present a reduced surge after stress in transcortin-deficient mice. No differences were detected between transcortin-deficient mice for anxiety-related traits. However, transcortin-deficient mice display increased immobility in the forced-swimming test and markedly enhanced learned helplessness after prolonged uncontrollable stress. The latter is associated with an approximately 30% decrease in circulating levels of free corticosterone as well as reduced Egr-1 mRNA expression in hippocampus in CBG-deficient mice. Additionally, transcortin-deficient mice show no sensitization to cocaine-induced locomotor responses, a well described corticosterone-dependent test. Thus, transcortin deficiency leads to insufficient glucocorticoid signaling and altered behavioral responses after stress. These findings uncover the critical role of plasma transcortin in providing an adequate endocrine and behavioral response to stress.
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Bodnar, Tamara S., Lesley A. Hill, Matthew D. Taves, Wayne Yu, Kiran K. Soma, Geoffrey L. Hammond, and Joanne Weinberg. "Colony-Specific Differences in Endocrine and Immune Responses to an Inflammatory Challenge in Female Sprague Dawley Rats." Endocrinology 156, no. 12 (September 24, 2015): 4604–17. http://dx.doi.org/10.1210/en.2015-1497.
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Sprague Dawley rats from different vendor colonies display divergent responses in a variety of experimental paradigms. An adjuvant-induced arthritis (AA) model of human rheumatoid arthritis was used to examine immune and endocrine responses to inflammatory challenge in Sprague Dawley rats from Charles River and Harlan colonies. Rats were injected with either complete Freund's adjuvant or physiological saline (control), weights, and paw volumes measured over 15 days, and blood and tissue were collected 16 days post-injection. Overall, Harlan rats developed more severe AA than Charles River rats. In addition, despite comparable corticosterone levels, corticosteroid binding globulin levels were lower in Harlan compared with Charles River rats in the absence of inflammation, suggesting that a lower corticosterone reservoir in Harlan rats may underlie their greater susceptibility to inflammation. With increasing AA severity, there was an increase in plasma corticosterone (total and free) and a decrease in corticosteroid binding globulin in both Charles River and Harlan rats. However, contrasting patterns of cytokine activation were observed in the hind paw, suggesting a reliance on different cytokine networks at different stages of inflammation, with Charles River rats exhibiting increased TNF-α, monocyte chemotactic protein-1 (MCP-1), keratinocyte chemoattractant/growth-regulated oncogene (KC/GRO), and IL-1β in the absence of clinical signs of arthritis, whereas Harlan had increased TNF-α, monocyte chemotactic protein-1, and IL-6 with mild to moderate arthritis. These colony-specific differences in endocrine and immune responses to AA in Sprague Dawley rats must be considered when comparing data from different laboratories and could be exploited to provide insight into physiological changes and therapeutic outcomes in arthritis and other inflammatory disorders.
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Scheuer, D. A., and S. W. Mifflin. "Chronic corticosterone treatment increases myocardial infarct size in rats with ischemia-reperfusion injury." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 6 (June 1, 1997): R2017—R2024. http://dx.doi.org/10.1152/ajpregu.1997.272.6.r2017.
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Experiments were conducted to determine the effect of chronic elevations in corticosterone on myocardial infarct size. Male Sprague-Dawley rats were treated for 7-22 days with corticosterone. Plasma corticosterone concentrations averaged 0.8 +/- 0.3 in control and 14.9 +/- 1.2 micrograms/dl in corticosterone-treated conscious rats. Experiments were performed in anesthetized rats. After a 30-min control period, myocardial ischemia (30 min)-reperfusion (3 h) was performed in control and corticosterone-treated rats. Mean arterial pressure (+/-SE) in control rats during control, ischemia, and reperfusion periods averaged 111 +/- 4, 100 +/- 5, and 94 +/- 4 mmHg (n = 6), respectively. Chronic treatment with corticosterone increased mean arterial pressure in all three periods 128 +/- 6, 117 +/- 7, and 109 +/- 7 mmHg; n = 8; P < 0.05). Infarct size (as % area at risk) was significantly larger in rats with chronic elevations in corticosterone compared with control rats (77 +/- 2 vs. 51 +/- 5%, P < 0.05). Acute (2 h) blockade of the glucocorticoid type II receptors with mifepristone antagonized the increases in arterial pressure and infarct size produced by chronic administration of corticosterone. Neither mifepristone nor acutely administered corticosterone affected arterial pressure or infarct size in rats without chronic corticosterone treatment. The effect of chronic elevations in plasma corticosterone concentration to increase infarct size could contribute to the increased risk of cardiovascular disease in clinical conditions associated with elevated glucocorticoid levels.