Soluble Corticosterone-Binding Macromolecules Extracted from Rat Brain

McEwen, Bruce S.; Magnus, Carew; Wallach, Gislaine

doi:10.1210/endo-90-1-217

Cited by 107 publications

(11 citation statements)

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“…Studies involving radiolabelled corticosterone indicate that this hormone reaches all parts of the brain in normal and adrenalec tomized rats [31]. However, both in vitro and in vivo studies indicate that the uptake and binding of corticosterone is es pecially great in the hippocampus, amygdala, and septum [15,20,23,29,30,31,39]. There were no apparent effects whatsoever of corticosterone implants at the hippocampus and amygdala in the present study.For the septal site, there was a significant trend when corticosterone in a liquid vehi cle was administered, but diffusion from the source was probable and difficult to monitor, whereas there was only a small nonsignificant effect when the beeswax pellet method was employed, where diffusion from the source was proba bly lesser.…”

Section: Discussioncontrasting

confidence: 60%

“…The proximity of the septal and preoptic sites may have had some bearing here. It also should be noted that some binding of corticosterone in hypothalamic tissue has been detected [23,29,30], corresponding to the most effective sites observed here. Indeed, recent evidence suggests substantial amounts of glucocortical receptors in the paraventricular hypothalamic nucleus [20,39], In a previous study [11], it was found that the regimens of hormone administration wherein corticosterone sup pressed lordosis all involved its delivery prior to that of es trogen.…”

Section: Discussionsupporting

confidence: 53%

“…Studies of uptake of radiolabelled corticosterone in dicate that this hormone reaches all parts of the brain in both normal and adrenalectomized rats, but that receptors are es pecially common in the hippocampus, amygdala, and sep tum [15,23,[29][30][31]39]. On the other hand, evidence indicates that lordosis behavior is dependent upon estrogen activity in the ventromedial nucleus of the hypothalamus and to a les ser extent the preoptic area [4,8,26,32].…”

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confidence: 99%

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Alteration of Estrogen-Induced Lordosis through Central Administration of Corticosterone in Adrenalectomized-Ovariectomized Rats

Catanzaro

1987

Neuroendocrinology

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Corticosterone was administered through various modes into several brain regions of estrogen-treated adrenalectomized-ovariectomized female rats. Daily administration of 20 µg corticosterone dissolved in propylene glycol through intracerebral cannulae effectively inhibited female sexual receptivity at each of four sites: third ventricle, ventromedial hypothalamus, preoptic area, and septum. Similar administration of lesser daily doses failed to inhibit receptivity. Implantation of pure crystalline corticosterone also had no effect on receptivity at any site. Beeswax pellets chronically releasing low doses of corticosterone significantly inhibited receptivity when implanted in the medial hypothalamus and preoptic area, with similar nonsignificant trends in the lateral septum and medial forebrain bundle, but had no effect in the dorsal hippocampus or the amygdala. The effective sites are similar to those in which estrogen activity is known to induce receptivity and those in which serotonergic activity is believed to inhibit receptivity, but do not entirely correspond to sites in the brain showing the greatest uptake of corticosterone.

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Section: Discussioncontrasting

confidence: 60%

Section: Discussionsupporting

confidence: 53%

mentioning

confidence: 99%

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Alteration of Estrogen-Induced Lordosis through Central Administration of Corticosterone in Adrenalectomized-Ovariectomized Rats

Catanzaro

1987

Neuroendocrinology

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“…Lower concentrations of receptor in some fetal tissues, however, could result from the relative deficiency or absence of receptor in certain cell types. In an adult rat, for example, McEwen (20) finds a severalfold variation in the extent of corticosterone uptake in different regions of the brain. In other tissues with relatively homogeneous cell populations, such as skeletal muscle and heart, this possibility seems less likely.…”

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confidence: 99%

Glucocorticoid Receptors and the Role of Glucocorticoids in Fetal Lung Development

Ballard

1972

Proc. Natl. Acad. Sci. U.S.A.

107

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The cellular mechanism of glucocorticoid effects upon fetal lung was examined in studies of specific binding'activity for corticosteroids. Cytoplasm of fetal rabbit lung contains receptor sites for [3Hjdexamethasone at a concentration of 0.43 + 0.04 'pmol/mg of cytosol protein, and the apparent dissociation constant for the binding reaction is 2.7 4± 0.4 nM. The ability of various steroids to compete with labeled dexamethasone for binding to receptor correlates with their biologic potency. The hormone-receptor complex formed in vitro at 00 binds with high affinity at 200 to isolated lung nuclei. It is estimated that there are 9500 nuclear binding sites and 12,000 cytoplasmic receptor sites per fetal lung cell.During the last 12 days of gestation in a rabbit, the concentration of cytoplasmic receptor in lung is constant and is 2-to 5-times greater than receptor-site concentration in fetal skin, kidney, heart, muscle, gut, liver, brain, thymus, and placenta. These findings demonstrate that the early steps in the mechanism of glucocorticoid action in target tissues are present in lung cells, and suggest that these hormones accelerate fetal lung differentiation and surfactant production in animals by the induction of new protein synthesis mediated by receptor.Adrenal glucocorticoids induce both morphological and enzymic changes in various target tissues. In fetal rabbit and lamb, these steroid hormones cause accelerated lung development and precocious appearance of pulmonary surfactant in whole-lung homogenates and lung washes (1)(2)(3) into cold isotonic phosphate-buffered saline (pH 7.6) and frozen at -20°for 0-2 days. Receptor activity was assayed in a cytosol fraction prepared at 20 by mincing tissue in one volume of medium 1 and then homogenizing with 6 strokes of a motor-driven (3000 rpm) Teflon pestle in a Duall Tissue Grinder (Kontes Glass Co.). The homogenate was centrifuged at 600 X g for 15 min, then at 100,000 X g for 60 min. Aliquots of the supernatant were added immediately to reaction mixtures containing [3H]dexamethasone at concentrations from 1 to 100 nM. Tubes containing in addition an excess of unlabeled dexamethasone (10 MM) were run in parallel for each [3H]dexamethasone concentration to determine "background" binding activity (6). Binding was complete by 90-120 min at 00, and was proportional to cytosol protein concentration between 2 and 20 mg/ml. Macromolecular bound radioactivity was determined by a charcoal assay (6) that utilizes the property of activated charcoal to absorb free, but not bound, steroid. Results are plotted as P3H]dexamethasone specifically bound (total radioactivity excluded from charcoal minus "background" counts) against free dexamethasone (total dexamethasone added minus the amount bound).Fetal lung nuclei were prepared from the 600 X g pellet by washing in medium 1 twice and once in medium 1 containing 0.25 M sucrose. Pellets of nuclei were combined with aliquots of cytosol previously incubated at 00 with a saturating concentration of PH]dexamethasone, with or ...

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“…McEwen, Weiss, and Schwartz 1969, McEwen, Magnus, and Wallach 1972, Gerlach and McEwen 1972; this finding has been replicated in other laboratories (Ford, Rhines, andSteig 1971, Knizley 1972). The binding of corticosterone, which is primarily nuclear McEwan 1972, Warembourg, 1975), appears to be maximal about one hour after injection , Ford et al 1971.…”

Section: Uptake Studiesmentioning

confidence: 53%