Abstract
The evidence indicating a specific abnormality of brain 5-HT function in depressed patients is reviewed. Biochemical studies have indicated that low plasma levels of tryptophan are unlikely to be the primary 'cause' of depression or of abnormal brain 5-HT function in depression. However, there may be a reduction of 5-HT synthesis or function in the brains of depressed patients and the uptake of 5-HT into platelets from depressed patients is consistently reduced. Neuroendocrine studies have suggested that various groups of depressed patients may exhibit different types of abnormal 5-HT-mediated responses. It is important to distinguish between the acute and chronic pharmacological effects of antidepressant treatment, which may account for the latency seen between onset of therapy and full clinical effect. Clinical studies have provided further evidence that 5-HT is implicated in the causation and treatment of depression, as both 5-HT precursors and selective inhibitors of 5-HT uptake are effective in the treatment of depression. Furthermore, inhibition of 5-HT synthesis can block the effect of antidepressant compounds. It is concluded that 5-HT function is decreased during depression, and that this carries important implications for the pharmacology of antidepressant drugs.
Published Version
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