Influence of hydrocoritsone and glucagon on liver tyrosine transaminase and on brain tyrosine, norepinephrine and serotonin.

Abstract

CURRENT hypotheses concerning biochemical origins of endogenous depression centre around serotonin (5HT)1 and norepinephrine2–4 changes in the brain. Recently, attempts have been made to relate disturbances in biogenic amine metabolism in the brain to metabolic factors outside the brain. Green and Curzon found5 that administration of hydrocortisone resulted in a decrease of 5HT in the brain (by way of an increase in tryptophan pyrrolase, the principal catabolic enzyme of tryptophan). This evidence gives strong support to the 5HT hypothesis of endogenous depression5,6. Takahashi et al. noted7 that after oral application of a tyrosine load there is a significant increase in the level of plasma tyrosine in maniacs and depressives as compared with control persons7. This increase is attributed to a reduced activity of α-ketoglutarate transaminase (TKT) (TKT is the principal catabolic enzyme of tyrosine) in patients with endogenous depression. Finally, patients with endogenous depression show a lower level of plasma tyrosine, phenylalanine, and tryptophan than normal subjects8. The reduction in the level of these amino-acids presumably leads to a disturbance in amine levels in the brain.