Precursor and end product effects upon indoleamine maturation in mouse brain.
The effects of tryptophan loading and the acid transport inhibitor, probenecid, on the maturation of 5-hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) have been studied in the maturing mouse brain. Tryptophan loading elevates already high endogenous tryptophan at all stages studied. It does not alter 5-HT or 5-HIAA at day 1 but does elevate levels of both at later stages. Probenecid does not affect 5-HT at any age or 5-HIAA at day 1, but does cause increasingly greater elevations of 5-HIAA at later stages. The results indicate that tryptophan-5-hydroxylase is substrate saturated in early postnatal stages but not later, and that the early postnatal brain lacks an acid transport mechanism for 5-HIAA egress but develops this at later stages.
D000367:Age Factors; D000818:Animals; D001921:Brain / Q000378:metabolism*; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism*; D051379:Mice; D011339:Probenecid / Q000494:pharmacology*; D012701:Serotonin / Q000378:metabolism*; D014364:Tryptophan / Q000378:metabolism / Q000494:pharmacology*
D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan; D011339:Probenecid