Abstract:
:Epinephrine (Epi) mediates various physiological effects via alpha2A-adrenergic receptors (alpha2A-ARs). Studies in mice with a point mutation in the gene for alpha2A-AR have shown that these receptors are responsible for the centrally mediated depressor effects of alpha2-AR agonists. These studies underscore the importance of understanding the basic cellular mechanisms involved in the expression of alpha2A-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 alpha2A-AR expression. These cells contain alpha2-ARs, which are predominately of the alpha2A-AR subtype. Our studies have shown that Epi causes a dose- and time-dependent decrease in steady-state levels of alpha2A-AR mRNA and number of alpha2A-ARs, effects that are mediated via alpha1- and beta-adrenergic receptors (alpha1-ARs and beta-ARs). These effects of Epi on alpha2A-AR mRNA and alpha2A-AR number are mimicked by activation of protein kinase C or increases in cellular cyclic AMP, which are intracellular messengers activated by alpha1-ARs and beta-ARs, respectively. Taken together, these results indicate that expression of alpha2A-ARs is regulated in a heterologous manner by Epi, via alpha1-AR- and beta-AR-mediated intracellular pathways.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Reutter MA,Richards EM,Sumners Cdoi
10.1046/j.1471-4159.1998.70010086.xsubject
Has Abstractpub_date
1998-01-01 00:00:00pages
86-95issue
1eissn
0022-3042issn
1471-4159journal_volume
70pub_type
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