Serotonin transport by blood platelets of depressive patients
Modai, I.; Aizenberg, D.; Hermesh, H.
Harefuah 110(2): 64-67
1986
ISSN/ISBN: 0017-7768 PMID: 3699599 Document Number: 275035
One of the most accepted theories of the etiology of depression involves brain serotonin activity. From a simple quantitative explanation which presumed reduced turnover of brain serotonin, the theory changed towards indirect modifications of pre and post-synaptic binding sites in accordance with the antidepressant effect of tricyclic medications. One of the most popular methods of measuring presynaptic serotonin receptors is the use of platelets due to similarities in their membrane function in relation to serotonin uptake. In schizophrenia, childhood psychosis, autism and anorexia nervosa, results of serotonin uptake by platelets are ambiguous and not helpful. However, in depressive patients, especially those with unipolar depression, less serotonin is transferred to blood platelets than in healthy individuals. The decreased uptake may be a reflection of a decreased number of binding sites, but with the same sensitivity. However, it is unclear whether this reduction reflects a general phenomenon or a difference in phase of the circadian serotonin rhythm from that in healthy individuals.