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Antidepressant research in the era of functional genomics: Farewell to the monoamine hypothesis

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Although blockade by antidepressants of monoamine uptake into nerve endings is one of the cornerstones of the monoamine hypothesis of depression, there is a clear discrepancy between the rapid effects of antidepressants in increasing synaptic concentrations of monoamine and the lack of immediate clinical efficiency of antidepressant treatment. Novel biological approaches beyond the 'monoamine hypothesis' are definitely expected to cause paradigm shifts in depression research. Functional genomics are powerful tools that can be used to identify genes affected by antidepressants or by other effective therapeutic manipulations. Using RNA fingerprinting technique, we have previously identified several cDNA fragments as antidepressant related genes and from these, original cDNA microarrays were developed. Some of these candidate genes may encode common functional molecules induced by chronic antidepressant treatment. Defining the roles of these genes in drug-induced neural plasticity is likely to transform the course of research on the biological basis of depression. Such detailed knowledge will have profound effects on the diagnosis, prevention, and treatment of depression.


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