Evidence for the presence of specific binding sites for corticoids in mouse liver plasma membranes

Abstract

The specific binding of [3H]cortisol to plasma membranes purified from mouse liver, studied by the ultrafiltration method, shows the existence of specific binding sites for cortisol. The kinetic parameters of this binding are KD = 4.4 nM and Bmax = 685 fmol/mg protein in presence of 1 microM of corticosterone. With respect to the binding of 4 nM [3H]cortisol to the membrane, the affinities of the steroids decreased in the following order: deoxycorticosterone greater than corticosterone greater than progesterone greater than cortisol greater than prednisolone greater than testosterone greater than 20 beta-hydroxyprogesterone greater than cortisone. Estradiol, dexamethasone, ouabain and triamcinolone acetonide do not have affinity for this binding site. Neither Ca2+ nor Mg2+ affected the binding of [3H]cortisol to the plasma membranes. Likewise, the presence of agonists and antagonists of alpha and beta-adrenergic receptors did not modify the binding of [3H]cortisol. The results suggest that the plasma membrane binding site characterized is more specific for corticoids and is different from nuclear glucocorticoid and progesterone receptors.

Specific binding sites for corticosterone in isolated cells and plasma membrane from rat liver

“…This Ko value is of the same order of magnitude that the one obtained by other authors with steroids and membranes (Suyemitsu & Terayama, 1975;Koch et al, 1978;Savart & Cabillic, 1985;Trueba et al, 1987Trueba et al, , 1989b. Based on K D and Bma x values and steroid affinities we can say that this high affinity site determined for [3H]corticosterone is possibly the same that was characterized previously with cortisol (Trueba et al, 1989b) and corticosterone in mouse liver (Trueba et al, 1989a).…”

“…On the other hand, binding sites or receptors for glucocorticoids have been reported for liver plasma membranes (Suyemitsu & Terayama, 1975;Allera, Rao & Breuer, 1980;Trueba et al, 1987;Quelle et al, 1988;Guendouz et al, 1988;Trueba et al, 1989b), pituitary gland Koch, Sakly & Lutz-Butcher, 1981), skeletal muscle (Savart & Cabiilic, 1985) and Xenopus oocytes (Sadler & Mailer, 1982;Sadler, Bower & Mailer, 1985). The [3H]corticosterone-hepatocyte binding shows a pattern for two independent types of sites.…”

“…In most of the experiments carried out to study glucocorticoid binding to isolated plasma membranes there is a common feature which supports their existence, distinct from the classical nuclear receptors (Suyemitsu & Terayama, 1975;Koch, 1978;Fant, Yeakley & Harrison, 1983;Omrani et al, 1983;Towle & Sze, 1983;Savart & Cabillic, 1985;Allera & Rao, 1986;Quelle et al, 1988). We have characterized the specific binding sites for cortisol in chicken and mouse (Trueba et al, 1989b) liver plasma membranes and corticosterone in mouse liver plasma membranes (Trueba et al, 1989a).…”

Nongenomic Steroid Action: Controversies, Questions, and Answers

“…In plasma membranes from chicken liver, mouse liver, and rat liver, specific binding sites for cortisol could be demonstrated (218,485,489). In rat liver plasma membranes, two types of binding sites for cortisol have been detected, a highaffinity site with low binding capacity and a low-affinity site with high binding capacity.…”

Hydrocortisone Impairs Hippocampal-Dependent Trace Eyeblink Conditioning in Post-Traumatic Stress Disorder

“…An extensive body of preclinical work confirms that glucose transport is inhibited following hydrocortisone administration. A more immediate effect is mediated through rapid membrane effects (Falkenstein et al, 2000;McEwen, 1997;Trueba et al, 1989), while a delayed action (4-12 h) is mediated through the glucocorticoid receptor (Horner et al, 1990;Munck, 1971;Virgin et al, 1991). Since the main goal of the study was to evaluate the sensitivity of the glucocorticoid receptors in PTSD, a longer time delay between administration of hydrocortisone and trace eye blink conditioning was chosen.…”