title: Diurnal differences in basal and acute stress levels of type I and type II adrenal steroid receptor activation in neural and immune tissues.
abstract: To examine diurnal differences in the proportions of receptors that were occupied and activated by basal and stress levels of corticosterone, we measured available type I (mineralocorticoid) and type II (glucocorticoid) adrenal steroid receptor levels in brain, pituitary, and immune tissues of unstressed and acutely stressed rats at the times of day when basal corticosterone secretion was at its trough [morning (AM)] and peak [evening (PM)]. In general, the estimated adrenal steroid receptor activation was greater in brain than in pituitary or immune tissue, and within a particular tissue, there was a greater degree of estimated activation of the adrenal steroid high affinity type I receptor than of the type II receptor. There was a greater activation of brain type II receptors by basal corticosterone in the PM (30-35%) than the AM (5-15%). As acute stress produced similar levels of receptor activation at both times of day (45-50%), the net change in type II receptor activation in the brain after acute stress was much smaller in the PM than in the AM. This suggests that there may be diurnal differences in the role of type II receptors in corticosterone negative feedback on the hypothalamic-pituitary-adrenal axis. In immune tissues, type II receptor activation by acute stress was especially heterogeneous, depending on both the immune compartment and the time of day, suggesting that these are important factors contributing to a differential impact of corticosterone on immune responses during acute stress. Taken together our results suggest that the tonic and phasic influences of corticosterone on target tissue responses very not only with the diurnal and stress secretion patterns of corticosterone, but also with target tissue factors, such as type I and type II receptor expression and hormone bioavailability. All of these factors contribute to considerable selectivity of action for the systemic hormone corticosterone.
authors.affiliation: Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021.
authors.forename: R L
authors.initials: RL
authors.lastname: Spencer
authors.forename: A H
authors.initials: AH
authors.lastname: Miller
authors.forename: H
authors.initials: H
authors.lastname: Moday
authors.forename: M
authors.initials: M
authors.lastname: Stein
authors.forename: B S
authors.initials: BS
authors.lastname: McEwen
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002940:Circadian Rhythm; D003345:Corticosterone / Q000097:blood; D003600:Cytosol / Q000378:metabolism; D007107:Immune System / Q000378:metabolism*; D008198:Lymph Nodes / Q000378:metabolism; D008297:Male; D010902:Pituitary Gland / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D018161:Receptors, Mineralocorticoid / Q000378:metabolism; D011987:Receptors, Steroid / Q000378:metabolism*; D013154:Spleen / Q000378:metabolism; D013312:Stress, Physiological / Q000378:metabolism*; D013950:Thymus Gland / Q000378:metabolism
chemical_list: D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D011987:Receptors, Steroid; D003345:Corticosterone