Abstract
THERE is general agreement that 5-hydroxytryptamine (5HT) is formed from 5-hydroxytryptophan (5HTP) in the presence of 5-hydroxytryptophan decarboxylase (5HTPD). It is then oxidized to 5-hydroxyindolylacetic acid (5HIAH) with monoamine oxidase (MAO). A number of theories have been suggested to explain the decrease of brain 5HT in experimental phenylketonuria1–3. First, the excessive phenylalanine might inhibit the hydroxylation of tryptophan in the liver4 or brain5, and thus reduce the amount of 5HTP available. Second, this excess might inhibit the active transport of tryptophan6 or 5HTP7–9 across the blood brain barrier or brain cell membrane. Third, the excess of phenylalanine and its metabolites might inhibit the decarboxylation of 5HTP10,11.
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YI-YUNG HSIA, D., JUSTICE, P., BERMAN, J. et al. Brain Serotonin in Experimental Tyrosinosis. Nature 202, 495–496 (1964). https://doi.org/10.1038/202495a0
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DOI: https://doi.org/10.1038/202495a0
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