November 1990

Autoradiographic Demonstration of Increased Serotonin 5-HT2 and β-Adrenergic Receptor Binding Sites in the Brain of Suicide Victims

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.

Arch Gen Psychiatry. 1990;47(11):1038-1047. doi:10.1001/archpsyc.1990.01810230054009

• 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.