Wirz-Justice A, Pühringer W, Lacoste V, Graw P, Gastpar M
Pharmakopsychiatr Neuropsychopharmakol. 1976 Nov;9(6):277-88. doi: 10.1055/s-0028-1094502.
In a precursor study with i.v. 1-5HTP (Ro 3-5940) after peripheral decarboxylase inhibition with benserazide (Ro 4-4602) in healthy human subjects the following biochemical changes were found: 1. Prolactin release was stimulated by benserazide alone, and further stimulated by 1-5HTP (more in women than in men). 2. Basal growth hormone secretion was not affected by benserazide, but was significantly stimulated by 1-5HTP, often to extremely high values. The time course of growth hormone release followed that of mood elevation in 8/11 subjects (and was even correlated in 3), providing data for speculation as to the interrelationships between affective state and neuroendocrinological function. 3. Cortisol levels were higher than normal throughout the experiment, but followed the diurnal decline. A late stimulation of cortisol release after 1-5HTP was observed. 4. The lack of increased platelet serotonin after 1-5HTP indicated efficacious peripheral decarboxylase inhibition by benserazide. 5. Benserazide treatment inhibited platelet MAO activity in certain subjects. Short-term increases in MAO activity after 1-5HTP were observed. 6. 1-5HTP displaced albumin-bound tryptophan by 20%.