[The neurobiology of depression]

Neurobiology dominates efforts to understand depression. This psychiatric illness is thought to result from dysfunctions in monoaminergic systems affecting norepinephrine, serotonin and dopamine. Abnormalities are linked to functional deficit of monoamines at several effector sites. Findings include reduced cerebrospinal fluid and urinary concentrations of metabolites, decreased plasma concentrations of precursors, modifications of receptor density and clinical effectiveness of drugs which increase neurotransmission in depressed patients. The original hypothesis of affective disorder envisaged a single transmitter model, but neuroscientific developments highlight the complexity of the central nervous system. Considerable evidence supports the hypothesis of combined alterations of monoaminergic functions and other systems like neuropeptides and neuroendocrine functions.