Rat C6 glioma cells contain type I as well as type II corticosteroid receptors.

Rat brain cytosol contains Type I corticosteroid receptors. Unlike Type II (glucocorticoid) receptors, Type I receptors have high affinity for the endogenous corticosteroids - aldosterone, deoxycorticosterone, and corticosterone - and much lower affinities for synthetic glucocorticoids. In the present study, we report that Type I corticosteroid receptors are present in C6 glioma cells. Type I receptors were identified in C6 cell cytosol and whole cells by the binding of [3H]aldosterone. The specific glucocorticoid RU 26988 was used to block Type II receptors. Measured in whole C6 cells, Type I receptors had a density of 2.1 +/- 1.1 fmol/10(6) cells and a dissociation constant (Kd) for [3H]aldosterone of 0.41 +/- 0.06 nM. The density of Type I receptors was only 2% of the density of Type II corticosteroid receptors (96 +/- 7 fmol/10(6) cells), measured in whole C6 cells by [3H]triamcinolone binding. The steroid specificity of glial cytosolic Type I receptors (deoxycorticosterone greater than corticosterone greater than aldosterone greater than dexamethasone greater than triamcinolone much greater than RU 26988) was identical to the steroid specificity of Type I receptors in rat brain cytosol. The potency of deoxycorticosterone was somewhat reduced when measured in whole cells. The steroid specificity of the Type I receptor differed markedly from that of the Type II (glucocorticoid) receptor (triamcinolone greater than dexamethasone greater than RU 26988 corticosterone greater than deoxycorticosterone greater than aldosterone). Since Type I receptors in the kidney mediate effects of aldosterone upon renal transport of sodium and potassium, it is proposed that glial Type I corticosteroid receptors may be involved in the regulation of glial ion transport.(ABSTRACT TRUNCATED AT 250 WORDS)