Regulation of Cyclic AMP Accumulation by Peptide Hormone Receptors in Immunocytochemically: Defined Astroglial Cells

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Abstract
Primary cultures of neonatal murine brain were reported to express multiple receptors that regulate adenylate cyclase activity. Since for the most part these results were obtained with mixed cell cultures, it was difficult to define receptor profiles for specific cell types. With this concern in mind a series of studies were designed to identify specific receptors present on highly purified, immunocytochemically defined astroglia derived from the cerebral cortices of neonatal rats. The capacity of a variety of peptide hormones to regulate cAMP metabolism in these cells was examined. Fibroblasts derived from the meninges represent a predictable source of contamination in primary CNS culture. To assign more clearly specific receptors to the astroglial cell population, receptor-mediated regulation of cAMP accumulation was also examined in fibroblasts. cAMP accumulation in astroglia was stimulated by catecholamines (acting at .beta.1-adrenergic receptors), prostaglandin E1, vasoactive intestinal polypeptide [VIP], .alpha.-MSH and ACTH. Bombesin, LHRH, neurotensin, TRH, somatostatin, secretin and vasopressin did not significantly increase cAMP levels in these cultures. Catecholamines, acting at .alpha.2-adrenergic receptors, and somatostatin inhibited agonist-stimulated cAMP accumulation. In meningeal cell cultures catecholamines (acting at .beta.2- and .alpha.2-adrenergic receptors) and prostaglandin E1 regulated cAMP levels. VIP did not stimulate and somatostatin did not inhibit cAMP accumulation in these cells.