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Article
September 1991

Desipramine Lowers Tritiated Para-Aminoclonidine Binding in Platelets of Depressed Patients

Author Affiliations

From the Departments of Psychiatry (Drs Piletz, Halaris, and Saran and Mr Marler), Neuroscience (Dr Piletz), and Pharmacology (Dr Halaris), Case Western Reserve University and the Departments of Psychiatry (Drs Piletz, Halaris, and Saran and Mr Marler), Neuroscience (Dr Piletz), and Pharmacology (Dr Halaris), Metro Health Medical Center, Cleveland, Ohio.

Arch Gen Psychiatry. 1991;48(9):813-820. doi:10.1001/archpsyc.1991.01810330037006
Abstract

• Platelet adrenergic receptor binding has been studied by several groups of investigators as a possible marker for depression and other psychiatric conditions. Although some of the findings have been discrepant, the results of the majority of studies that have used imidazoline compounds as ligands have confirmed elevated α2—adrenergic receptor binding in depression. We have emphasized the advantages of obtaining platelet-purified plasma membranes and using tritiated para-aminoclonidine as the ligand of choice. By using "site-selective" concentrations of tritiated paraaminoclonidine, we have identified two high-affinity— binding sites of the platelet α2—adrenergic receptor that appear to be upregulated in depression before treatment. Depressed patients were treated with desipramine hydrochloride for 6 to 8 weeks, and platelet binding was reassessed. Desipramine reduced binding to nearly normal levels at both site-selective concentrations of tritiated para-aminoclonidine. The concentrations of plasma catecholamines could play a role in the downregulation of binding at posttreatment. We discuss these findings in the context of platelet imidazoline-binding sites being a possible state-dependent marker for depression.

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