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Changes in the platelet intracellular calcium response to serotonin in patients with major depression treated with electroconvulsive therapy: state or trait marker status.
journal contributionposted on 2000-03-01, 00:00 authored by H Plein, Michael BerkMichael Berk
Platelet serotonin type 2A receptor (5-HT2A) sensitivity changes have previously been documented in depression, although it is unclear if this represents a stable trait marker of the illness, or whether it represents an acute state marker of depression that would change with treatment. Electroconvulsive therapy (ECT) may be a useful intervention to separate out trait and state marker status avoiding the potential confounding effects of pharmacotherapy on receptor function. Using spectrofluorometry, the platelet 5HT2A, receptor sensitivity as reflected by the intracellular calcium response to serotonin stimulation, was measured every week in patients suffering from major depression and undergoing ECT. There was a significant drop in the platelet response to serotonin stimulation over a course of ECT, with an associated progressive decrease in Hamilton Rating Scale of Depression (HAM-D) scores. This may suggest either decreased sensitivity of platelet 5HT2A receptors as a mechanism of action of ECT, or changes in second messengers such as the inositide phospholipid system. This suggests that the enhanced sensitivity of platelet 5HT2A receptors may be a state marker of major depression.
JournalInternational Clinical Psychopharmacology
Pagination93 - 98
PublisherLippincott, Williams & Wilkins
Publication classificationC1.1 Refereed article in a scholarly journal
Copyright notice2000, Lippincott, Williams & Wilkins
AdolescentAdultAgedBiological MarkersBlood PlateletsCalciumDepressive DisorderElectroconvulsive TherapyFemaleHumansIntracellular FluidMaleMiddle AgedReceptors, SerotoninScience & TechnologyLife Sciences & BiomedicinePharmacology & PharmacyPsychiatryperipheral markerplateletreceptorserotonin5-HT2 RECEPTOR-BINDINGANTIDEPRESSANT TREATMENTSBLOOD-PLATELETSUP-REGULATIONBRAINDRUGSFENFLURAMINEMECHANISMPROLACTINNEURONS