Adrenal steroid receptor binding in spleen and thymus after stress or dexamethasone.
Journal Article
Overview
abstract
Type I and II adrenal steroid receptor binding was measured in spleen and thymus of adrenalectomized (ADX) rats and intact rats at basal levels of corticosterone after 1 h of restraint stress or after exogenous administration of dexamethasone (DEX). Concurrent receptor determinations were made in the hippocampus and pituitary. Receptor binding measures in immune tissues and pituitary were less responsive to varying levels of endogenous hormones than binding measures in hippocampus. Compared with ADX rats, type I binding in spleen and pituitary of intact rats at basal levels of corticosterone was unchanged, whereas type I binding in the hippocampus was significantly decreased. Furthermore, despite peak levels of corticosterone, type II binding in spleen, thymus, and pituitary of stressed rats was also unchanged, whereas type II binding in the hippocampus of stressed animals was significantly lower. In contrast, DEX, a well-known immunosuppressant, reduced type II binding in immune tissues more than in the hippocampus. Because a decrease in receptor binding measured in vitro may reflect receptor activation in vivo, these results suggest that there may be considerable heterogeneity in the degree of activation of adrenal steroid receptor subtypes in immune, pituitary, and hippocampal tissue by endogenous and exogenous glucocorticoids.