Precursor and End Product Effects upon Indoleamine Maturation in Mouse Brain

The results indicate that tryptophan-5-hydroxylase is substrate saturated in early postnatal stages but not later, and that theEarly postnatal brain lacks an acid transport mechanism for 5-HIAA egress but develops this at later stages.

Abstract

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.