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Prostaglandins, Platelets, and Schizophrenia
John Rotrosen, MD;
Arthur D. Miller;
Donna Mandio;
L. J. Traficante, PhD;
Samuel Gershon, MD
Arch Gen Psychiatry. 1980;37(9):1047-1054.
Abstract
• Prostaglandin (PG) E, enhances formation of 3H-adenosine3',5'-cyclic monophosphate (3H-cAMP) in platelets pulse-labeled with 3H-adenine. This response was assessed as an index of receptor sensitivity and of PG function. Prostaglandin E1 lated 3H-cAMP accumulation in platelets from schizophrenics was significantly reduced compared with control subjects. Platelet incorporation of 3H-adenine and basal 3H-cAMP levels did not differ between groups. Psychotropic drugs added in vitro generally did not alter basal or PGE1-stimulated 3H-cAMP accumulation. We discuss the results in terms of the possible role of PGs in the etiopathology of schizophrenia and derivative implications for treatment.
Author Affiliations
From the Neuropsychopharmacology Research Unit, Department of Psychiatry, New York University School of Medicine, New York.
Footnotes
Accepted for publication March 23, 1979.
Reprint requests to Neuropsychopharmacology Research Unit, Department of Psychiatry, New York University Medical Center, 550 First Ave, New York, NY 10016 (Dr Rotrosen).
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