Platelet 5-HT2A-receptor-mediated induction of aggregation is not altered in major depression
Article first published online: 22 AUG 2002
Copyright © 2002 John Wiley & Sons, Ltd.
Human Psychopharmacology: Clinical and Experimental
Volume 17, Issue 8, pages 419–424, December 2002
How to Cite
Gómez-Gil, E., Gastó, C., Díaz-Ricart, M., Carretero, M., Salamero, M., Catalán, R. and Escolar, G. (2002), Platelet 5-HT2A-receptor-mediated induction of aggregation is not altered in major depression. Hum. Psychopharmacol. Clin. Exp., 17: 419–424. doi: 10.1002/hup.429
- Issue published online: 27 NOV 2002
- Article first published online: 22 AUG 2002
- Manuscript Accepted: 22 JUL 2002
- Manuscript Received: 6 JUN 2002
- Hospital Clinic, Barcelona, Spain
- major depression;
- 5-HT2A receptor;
- 5-HT receptor function;
- platelet aggregation
Studies of the 5-HT2A 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-HT2A receptor pathway in platelets.
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-HT2A platelet receptors mediate the serotonin-induced platelet aggregation response, this index was used as a measure of the functional status of the platelet 5-HT2A receptor pathway.
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.
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-HT2A receptors in major depression. Copyright © 2002 John Wiley & Sons, Ltd.