Affective disorders and aggression disorders: evidence for a common biological mechanism.
Ever since the discovery that the classical antidepressants--tricyclics and MA oxidase inhibitors--exert an influence on central 5-HT, this neurotransmitter has been studied in depression, particularly in those forms responsive to this type of treatment. This chapter reviews the evidence in favor of a relationship between depression and central 5-HT dysfunctions. Most of the findings have been derived from patients with depression as the principal diagnosis. Some data have originated from patients suffering from a somatic illness and from depression as well. Both peripheral and central data are discussed. Although no single 5-HT-related finding in depression has so far been unequivocally established, the available evidence, in balance, justifies the tentative conclusion that disturbances in 5-HT metabolism can occur in depression. Lowered CSF 5-HIAA, the major indicator of disturbed central 5-HT metabolism in depression, has also been reported in aggression disorders, both in patients who had committed suicidal acts and in those with outward-directed aggression. The finding can not be explained by a concomitant state of depression. Rather than to discard the classical 5-HT-depression hypothesis, in favor of a 5-HT-aggression hypothesis, the hypothesis is launched that disturbances in serotonergic regulation can give rise to both mood and aggression disorders. This would provide a biological explanation for the clinical observation that those disorders frequently go hand in hand.
D006916:5-Hydroxytryptophan / Q000627:therapeutic use; D000374:Aggression / Q000502:physiology*; D001792:Blood Platelets / Q000378:metabolism; D002352:Carrier Proteins; D002446:Celiac Disease / Q000503:physiopathology; D003866:Depressive Disorder / Q000134:cerebrospinal fluid / Q000378:metabolism*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D006897:Hydroxyindoleacetic Acid / Q000134:cerebrospinal fluid; D008297:Male; D010300:Parkinson Disease / Q000503:physiopathology; D011388:Prolactin / Q000378:metabolism; D011955:Receptors, Drug; D017981:Receptors, Neurotransmitter / Q000502:physiology; D011985:Receptors, Serotonin / Q000502:physiology; D012701:Serotonin / Q000378:metabolism*; D013405:Suicide; D014364:Tryptophan / Q000097:blood
D002352:Carrier Proteins; D011955:Receptors, Drug; D017981:Receptors, Neurotransmitter; D011985:Receptors, Serotonin; C027775:imipramine receptor; D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan; D011388:Prolactin; D006916:5-Hydroxytryptophan; D006854:Hydrocortisone