Abstract
Common wisdom presently suggests that the neurobiological basis for therapies of sleep disorders with oral loading doses of L-tryptophan (TRP) is the increase in synthesis, storage and/or release of serotonin (5-HT) in syn-aptosomal compartments from TRP transported from plasma to central neurons. Quantitatively, the conversion of TRP to 5-HT and/or biologically active in-dole derivatives in brain structures is very small compared to tryptophan oxidation in the periphery through both dioxygenases (indole 2, 3-dioxygenase in lung, intestine and other organs and liver tryptophan 2, 3-dioxygenase). Therefore, the elucidation of strategies leading to an increased transport of the administered TRP dose into the brain and thus utilization within neurons is of considerable importance.
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© 1991 Plenum Press, New York
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Demisch, L., Kaczmarczyk, P. (1991). Tryptophan Metabolism in Healthy Subjects: Influence of Pyridoxine after Single or Repeated Administrations. In: Schwarcz, R., Young, S.N., Brown, R.R. (eds) Kynurenine and Serotonin Pathways. Advances in Experimental Medicine and Biology, vol 294. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5952-4_58
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DOI: https://doi.org/10.1007/978-1-4684-5952-4_58
Publisher Name: Springer, Boston, MA
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