Platelet serotonin studies in affective disorders: evidence for a serotonergic abnormality?

Abstract

This chapter considers four types of studies of platelet serotonergic measures in affective disorders: active 5-HT uptake, [3H]imipramine binding, [3H]paroxetine binding, and 5-HT2 binding site or receptor studies. Various abnormalities of serotonergic processes have been demonstrated in patients with major depression or in post-mortem specimens from depressed patients or suicides. The most direct evidence of this type involves measurement of brain 5-hydroxytryptamine (5-HT, serotonin), its major metabolite 5-hydroxyindoleacetic acid (5-HIAA), or brain 5-HT receptor and [3H]imipramine-binding (IB) sites in suicides or deceased depressed patients. Less direct measures of serotonergic function in depression include studies of cerebrospinal fluid (CSF) 5-HIAA concentration, plasma tryptophan in relation to the concentrations of large neutral amino acids, and the hormone and behavioural responses to challenges with tryptophan, 5-hydroxytryptophan (5-HTP), various direct 5-HT agonists, such as raeta-chlorophenylpiperazine (m-CPP), buspirone, 6-chloro- 2-[l-piperazinyl]pyrazine (MK 212) or fenfluramine, a 5-HT releaser. Perhaps the most indirect means of studying a possible disturbance of serotonergic mechanisms in depression involves the blood platelet, which is the subject of this chapter.