Abstract

The rate of serotonin synthesis has hitherto been measured by two different methodological approaches, steady- and nonsteady-state. In these methods, the rate of synthesis is estimated from the change in the concentration of a tryptophan metabolite after inhibition of an enzyme (tryptophan hydroxylase, aromatic amino acid decarboxylase (AAAD) or monoamine oxidase) or the inhibition of 5-hydroxyindoleacetic acid transport. These approaches can be challenged on the grounds that a feedback mechanism might have some effect on the measured synthesis rate. A major disadvantage of these methods is the necessity of separating different metabolites, a time-consuming process that generally requires tissue sampling, which is usually heterogeneous. Both pharmacological manipulation and tissue sampling have a profound effect on the estimation of the synthesis rates in all brain structures.

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