Effect of ADP on PGE₁Formation in Blood Platelets from Patients with Depression, Mania and Schizophrenia

Abstract

Adenosine diphosphate (ADP) stimulates the synthesis of prostaglandin E1 (PGE1) in lysed platelets from normal subjects, patients with affective illness but not in platelets from cases of schizophrenia. The stimulation is concentration-dependent and follows a curve which is mildly sigmoid in the normal, markedly sigmoid in depression and hyperbolic in mania.

Omega-3 Fatty Acids: Role in the Prevention and Treatment of Psychiatric Disorders

“…Thus, there will be a flip from excess formation of free PUFA and PGs to reduced formation. The evidence of enhanced PGE1 production in mania and depressed PGE1 production in depression would be in line with this hypothesis [108]. Therefore, if PUFA and their derivatives are important in regulating mood, this may explain the mood changes in bipolar disorder.…”

Elevated plasma prostaglandin E2 levels in schizophrenia

“…Other studies have also demonstrated a reduced sensitivity of schizophrenic platelets to PGEI (Kafka et al, 1979(Kafka et al, , 1983(Kafka et al, , 1986Rotrosen et al, 1980;Garver et al, 1982;Kanof et al, 1986). Since a decrease in PGE1 leads to hyposensitivity of the receptor (Vincent et al, 1974) Abdulla and Hamadah (1975) have shown a dramatic reduction in ADP-stimulated PGEt formation m platelet membrane of schizophrenics. PGE~ deficiency may cause excess PGE2, because a primary fall in PGE1 formation will lead to increased arachidonic acid mobilization and enhanced formation of PGE2 (Horrobin, 1980).…”

CNS signal transduction in the pathophysiology and pharmacotherapy of affective disorders and schizophrenia

“…Reexamining these earlier reports suggests an alternative explanation for the alterations in membrane phospholipids observed, that these phospholipid changes may be reflections of, or antecedents to, disturbances in transmembrane signal transduction in SCZ. In support of this notion, prostaglandin formation, which arises from phospholipid precursors, has been found to be much lower in platelets from SCZ patients (Abdulla and Hamadah, 1975). In addition, the activity of platelet PLA,, a key enzyme in the conversion of membrane phospholipids to eicosanoid second messengers, has been reported to be increased in unmedicated SCZ patients and normalized after treatment (Gattaz et al, 1987(Gattaz et al, , 1990.…”