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Regulation of α 2A ‐Adrenergic Receptor Expression by Epinephrine in Cultured Astroglia from Rat Brain
Author(s) -
Reutter Michael A.,
Richards Elaine M.,
Sumners Colin
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.70010086.x
Subject(s) - second messenger system , receptor , adrenergic receptor , epinephrine , intracellular , endocrinology , medicine , messenger rna , biology , adrenergic , signal transduction , microbiology and biotechnology , gene expression , chemistry , gene , biochemistry
Epinephrine (Epi) mediates various physiological effects via α 2A ‐adrenergic receptors (α 2A ‐ARs). Studies in mice with a point mutation in the gene for α 2A ‐AR have shown that these receptors are responsible for the centrally mediated depressor effects of α 2 ‐AR agonists. These studies underscore the importance of understanding the basic cellular mechanisms involved in the expression of α 2A ‐ARs, of which little is known. We use astroglia cultured from the hypothalamus and brainstem of adult Sprague‐Dawley rats as a model system in which to study factors that regulate α 2A ‐AR expression. These cells contain α 2 ‐ARs, which are predominately of the α 2A ‐AR subtype. Our studies have shown that Epi causes a dose‐ and time‐dependent decrease in steady‐state levels of α 2A ‐AR mRNA and number of α 2A ‐ARs, effects that are mediated via α 1 ‐ and β‐adrenergic receptors (α 1 ‐ARs and β‐ARs). These effects of Epi on α 2A ‐AR mRNA and α 2A ‐AR number are mimicked by activation of protein kinase C or increases in cellular cyclic AMP, which are intracellular messengers activated by α 1 ‐ARs and β‐ARs, respectively. Taken together, these results indicate that expression of α 2A ‐ARs is regulated in a heterologous manner by Epi, via α 1 ‐AR‐ and β‐AR‐mediated intracellular pathways.