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Depression is a mood disorder characterized by complex alterations of neurotransmitters such as serotonin, norepinephrine, and dopamine. In particular, there is substantial evidence of abnormalities in serotonin neurotransmission. Peripheral parameters of serotoninergic transmission, such as the 5-hydroxytryptamine content of plasma and platelets, have been used to identify biochemical alterations related to depression. In recent years, these parameters have also been used to examine the mechanism of action of antidepressive drugs such as the selective serotonin reuptake inhibitors. This study investigated the interaction between the plasma and platelet levels of fluoxetine and serotonin after fluoxetine administration to depressed patients. Twelve patients affected by major depression (according to the DSM-IV criteria) received a single oral dose of fluoxetine in the morning: 5 mg in the first 5 days, 10 mg from day 6 to day 10, and 20 mg from day 11 to day 40. Blood samples were collected at 0, 7, 10, and 24 hours after drug administration on the day 1 of fluoxetine 5 mg and on the 1st and the 30th day of fluoxetine 20 mg (days 11 and 40 of treatment, respectively). Plasma fluoxetine and serotonin levels increased after drug administration, reaching the highest levels on the 30th day of fluoxetine 20 mg. Fluoxetine levels were also detectable in platelets, with a time variation similar to plasma values. Platelet serotonin levels decreased after drug administration, and the lowest values were observed on the 30th day of fluoxetine 20 mg.

Pain and depression may share common neurochemical substrates, therefore the study of pain sensation in depression might be valuable in the investigation of the pathophysiology of depression itself. In order to investigate the sensation of pain in depression, we measured pain threshold and sensory threshold by means of a dental tester, comparing a group of depressed patients with healthy volunteers. The results showed the presence of a higher sensory threshold and pain threshold in patients than in controls. This may be related to a hyperfunction of the opiate system, which in turn might be primary or secondary to a decreased modulatory function of other neurotransmitters, in particular of serotonin, whose abnormalities in depressive states are well-documented.

Psychiatrists have always maintained that there is a relationship between aggressive behaviour and suicide in depressed patients. However, this relationship is based on inconsistent and undocumented hypotheses, not on reliable clinical experimental data. The present study was designed to investigate the relationship between aggressive behaviour assessed by means of the Buss and Durkee Hostility Inventory (BDHI), and suicide in a sample of 134 depressed out-patients. The group with a higher level of suicidal behaviour was of younger age. The association between depressive subtypes (major depression, recurrent; major depression, single episode; bipolar disorder, depressive episode; dysthymia) and suicidality was found to be statistically significant. In contrast, there was no correlation between depressive subtypes and aggressive behaviour. The relationship between suicide and guilt as measured by the BDHI suggests that, in depression, suicidal behaviour becomes part of a symptom pattern in which aggression does not appear to be the main component. The suicide dimension arises when the cognitive sphere is involved. In fact, in depression, suicide is included among the cognitive disturbances, together with guilt, paranoid and obsessive-compulsive symptoms, depersonalization/derealization and agitation.