Corticotropin-releasing hormone and dexamethasone do not alter secretion of immunoreactive beta-endorphin from dissociated fetal hypothalamic cell cultures

Corticotropin-releasing hormone (CRH) and glucocorticoids are major regulators of the hypothalamic-pituitary-adrenal (HPA) axis controlling secretion of beta-endorphin and other pro-opiomelanocortin (POMC)-derived peptides from pituitary. Although previous work has shown that CRH stimulates secretion of beta-endorphin from adult hypothalamic explants, and that glucocorticoids can inhibit basal and stimulated secretion of POMC-derived peptides from pituitary, the role of glucocorticoids on hypothalamic beta-endorphin secretion is not known. Studies were performed to assess the effects of CRH and dexamethasone, a potent glucocorticoid, on secretion of immunoreactive (IR) beta-endorphin from dissociated fetal hypothalamic cell cultures. CRH (10(-9)-10(-6) M) did not stimulate secretion of IR-beta-endorphin from hypothalamic cells which did release IR-beta-endorphin upon potassium-induced depolarization. However, CRH did stimulate IR-beta-endorphin secretion from fetal hypothalamic explants which were similar to hypothalamic tissue from which dissociated hypothalamic cell cultures were derived. Exposure of cells to dexamethasone (10(-6) M) did not inhibit basal or potassium-stimulated release of IR-beta-endorphin. These results indicate that: (1) dissociated fetal hypothalamic cells in culture do not exhibit a functional CRH receptor coupled to stimulation of IR-beta-endorphin secretion; (2) exposure of hypothalamic cells to dexamethasone does not inhibit basal nor depolarization-induced release of IR-beta-endorphin; and (3) dissociated fetal hypothalamic cells may have limited utility in elucidating specific regulatory relationships because of in vitro conditions and/or cytoarchitectural relationships.