Cortisol 17 beta acid, transcortin, and the heterogeneity of rat brain glucocorticoid receptors.
Binding of tracer or competing steroids to transcortin can compromise specificity studies on receptors for adrenal steroids. Recently Alexis et al. have used cortisol 17 beta acid at high concentrations to prevent steroid binding to any transcortin possibly contaminating rat brain cytosol preparations. On the basis of limited specificity studies of [3H]dexamethasone and [3H]corticosterone binding under such conditions, it was claimed that binding sites for the two steroids are indistinguishable, and it is thus unnecessary to invoke distinct binding sites for each glucocorticoid. We have extended these competition studies in the presence of cortisol 17 beta acid, and shown that in rat hippocampus Type I, corticosterone-preferring glucocorticoid receptors can be clearly distinguished both from transcortin and from Type II, dexamethasone-binding glucocorticoid receptors.
D000732:Androstanols / Q000494:pharmacology; D000818:Animals; D001667:Binding, Competitive; D001923:Brain Chemistry; D003345:Corticosterone / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism; D005260:Female; D006854:Hydrocortisone / Q000031:analogs & derivatives* / Q000378:metabolism; D066298:In Vitro Techniques; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000032:analysis*; D014156:Transcortin / Q000378:metabolism*
D000732:Androstanols; D011965:Receptors, Glucocorticoid; C049873:cortisol-17 acid; C038341:RU 26988; D003907:Dexamethasone; D014156:Transcortin; D003345:Corticosterone; D006854:Hydrocortisone