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Platelet 5-HT2A-receptor-mediated induction of aggregation is not altered in major depression
Esther Gómez-Gil1, Cristóbal Gastó, Maribel Díaz-Ricart
1Instituto Clínic de Psiquiatría y Psicología, Hospital Clínic, Institut d'investigacions Biomediques August Pi i Sunyer (IDIBAPS), Faculty of Medicine, University of Barcelona, Villaroel 170, 08036 Barcelona, Spain. esgomez@clinic.ub.es
Background:
Studies of the 5-HT(2A) receptor subtype in major depression have focused on the density of these receptors in neuronal cells and platelets, showing an up-regulation secondary to a deficit in serotonergic activity in major depression. However, their functional state has often been disregarded. The aim of the study was to investigate whether depressed patients show abnormalities in the function of the 5-HT(2A) receptor pathway in platelets.
Method:
The percentage of serotonin-amplified platelet aggregation to adenosine diphosphate (ADP) was assessed in 30 untreated patients with major depressive disorder and in 15 controls. Since 5-HT(2A) platelet receptors mediate the serotonin-induced platelet aggregation response, this index was used as a measure of the functional status of the platelet 5-HT(2A) receptor pathway.
Results:
There was no significant difference in the percentage of serotonin-amplified platelet aggregation to ADP between depressed patients and controls. No correlation with the severity of depression, as assessed by the Hamilton scale, was found.
Conclusion:
The results showed no consistent changes in the platelet aggregating responses to serotonin in the depressed patients. Therefore this study does not support the hypothesis of an alteration of the functional status of platelet 5-HT(2A) receptors in major depression.