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Victoria Arango, PhD; Paul Ernsberger, PhD; Peter M. Marzuk, MD; Jaw-Sy Chen, PhD; Helen Tierney, MD; Michael Stanley, PhD; Donald J. Reis, MD; J. John Mann, MD

Arch Gen Psychiatry. 1990;47(11):1038-1047.

Abstract
• Suicidal behavior has been linked to a deficiency in serotonin neurotransmission, but it is not known which brain regions are involved. We determined the pattern of alteration in serotonin 5-HT₂ (5-HT₂) receptor binding sites in suicide victims in prefrontal cortex compared with temporal cortex using a matched-pairs design to study 11 suicide victims and 11 matched controls, by both membrane binding and quantitative receptor autoradiography. Since a relationship between the serotonergic and noradrenergic systems has been proposed, we also examined β-adrenergic receptor binding sites. Binding to 5-HT₂ and β-adrenergic sites in slide-mounted sections correlated strongly with binding site number in membrane preparations. A specific laminar distribution of 5-HT₂ binding sites was found in both the control and suicide groups, whereas β-adrenergic binding sites did not differ across cortical layers. A significant increase was found in suicide victims across all cortical layers in both receptor subpopulations in the prefrontal cortex, but only β-adrenergic sites were increased in the temporal cortex. We conclude that suicide is associated with a localized increase in 5-HT₂ binding sites.

Author Affiliations
From the Laboratory of Psychopharmacology, Department of Psychiatry (Drs Arango, Marzuk, Chen, Tierney, and Mann), and Division of Neurobiology, Department of Neurology (Drs Arango, Ernsberger, and Reis), Cornell University Medical College, and the Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University (Dr Stanley), New York, NY. Drs Arango and Mann are now with the Laboratories of Neuropharmacology, Department of Psychiatry, University of Pittsburgh (Pa). Dr Ernsberger is now with the Division of Hypertension, Case Western Reserve University, Cleveland, Ohio.

Footnotes
Accepted for publication February 13, 1990.

This study was presented in part at the American Psychiatric Association Annual Meeting, Montreal, Canada, May 11, 1988; and the Society for Neuroscience Annual Meetings, New Orleans, La, November 17, 1987, and Toronto, Ontario, November 14, 1988.

Reprint requests to Laboratories of Neuropharmacology, Western Psychiatric Institute and Clinic, W1645 Biomedical Science Tower, University of Pittsburgh, 3811 O'Hara St, Pittsburgh, PA 15213 (Dr Arango).

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