Abstract:
:Antidepressant drugs remain poorly understood, especially with respect to pharmacological mechanisms of action. This lack of knowledge results from the extreme complexity inherent to psychopharmacology, as well as to a corresponding lack of knowledge regarding depressive disorder pathophysiology. While the final analysis is likely to be multifactorial and heterogeneous, compelling evidence exists for upregulation of brain α2 adrenergic receptors (ARs) in depressed patients. This evidence has sparked a line of research into actions of a particular antidepressant drug class, the tricyclic antidepressants (TCAs), as direct ligands at α(2A)ARs. Our findings, as outlined herein, demonstrate that TCAs function as arrestin-biased ligands at α(2A)ARs. Importantly, TCA-induced α(2A)AR/arrestin recruitment leads to receptor endocytosis and downregulation of α(2A)AR expression with prolonged exposure. These findings represent a novel mechanism linking α(2)AR trafficking with antidepressant pharmacology.
journal_name
Prog Mol Biol Transl Scijournal_title
Progress in molecular biology and translational scienceauthors
Cottingham C,Ferryman CJ,Wang Qdoi
10.1016/bs.pmbts.2015.03.007subject
Has Abstractpub_date
2015-01-01 00:00:00pages
207-25eissn
1877-1173issn
1878-0814pii
S1877-1173(15)00060-5journal_volume
132pub_type
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journal_title:Progress in molecular biology and translational science
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