Association Between Serotonin Transporter Gene Promoter Polymorphism(5HTTLPR) and Behavioral Responses to Tryptophan Depletion in Healthy Women With and Without Family History of Depression

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Abstract
THE INVOLVEMENT of serotonergic pathways in the pathogenesis of unipolar depression has been the subject of intensive research for many years. There is now substantial evidence suggesting that altered brain serotonergic transmission plays a key role in the development of depression.1 Altered serotonin system indexes, including lower plasma tryptophan levels,2,3 reduced cerebrospinal fluid 5-hydroxyindoleacetic acid levels,4 decreased platelet serotonin uptake,5 and blunted neuroendocrine responses in challenge studies of different serotonin receptors suggesting decreased brain serotonin responsiveness,6-9 have been reported in depressed patients relative to healthy control subjects. Moreover, brain imaging studies suggest widespread impairment of serotonergic function in depression.10,11