Alpha 2.0
Login Register
» Articles » PMID: 24194047

The Relationships Between the Availability OfL-tryptophan to the Brain, the Spontaneous HPA-axis Activity, and the HPA-axis Responses to Dexamethasone in Depressed Patients

Overview
Journal Amino Acids
Specialty Biochemistry
Date 2013 Nov 7
PMID 24194047
Citations 4
Authors
M Maes
B Minner
E Suy
Affiliations
Soon will be listed here.
Abstract

The present study was conducted in order to investigate the negative relationships between measures of hypothalamic-pituitary-adrenal (HPA)-axis activity and the availability of L-tryptophan (L-TRP) to the brain in depressive patients. To this end we measured the following: plasma total L-TRP, the ratio of L-TRP to the sum of competing amino acids (CAA), free urinary cortisol (UFC) excretion in 24 hr urine samples, and the 8 a.m. postdexamethasone cortisol levels. We found that the availability of L-TRP to the brain was significantly negatively correlated with the postdexamethasone cortisol values. Cortisol nonsuppressors averaged significantly lower L-TRP and L-TRP/CAA values compared to suppressors. No significant relationship was established between the availability of L-TRP and UFC excretion. It is concluded that the availability of L-TRP is related to the actual alterations in cortisol induced by dexamethasone rather than with the spontaneous baseline HPA-axis activity.

Citing Articles

Tryptophan catabolites, inflammation, and insulin resistance as determinants of chronic fatigue syndrome and affective symptoms in long COVID.

Al-Hakeim H, Abed A, Moustafa S, Almulla A, Maes M Front Mol Neurosci. 2023; 16:1194769.

PMID: 37333619 PMC: 10272345. DOI: 10.3389/fnmol.2023.1194769.

The tryptophan catabolite or kynurenine pathway in major depressive and bipolar disorder: A systematic review and meta-analysis.

Almulla A, Thipakorn Y, Vasupanrajit A, Algon A, Tunvirachaisakul C, Hashim Aljanabi A Brain Behav Immun Health. 2022; 26:100537.

PMID: 36339964 PMC: 9630622. DOI: 10.1016/j.bbih.2022.100537.

Neuroinflammation and comorbidity of pain and depression.

Walker A, Kavelaars A, Heijnen C, Dantzer R Pharmacol Rev. 2013; 66(1):80-101.

PMID: 24335193 PMC: 3880465. DOI: 10.1124/pr.113.008144.

Effects of acute tryptophan depletion on affective processing in first-degree relatives of depressive patients and controls after exposure to uncontrollable stress.

Firk C, Markus C Psychopharmacology (Berl). 2008; 199(2):151-60.

PMID: 18551283 PMC: 2493867. DOI: 10.1007/s00213-008-1125-8.

References
1.
Carroll B, Curtis G, MENDELS J . Neuroendocrine regulation in depression. II. Discrimination of depressed from nondepressed patients. Arch Gen Psychiatry. 1976; 33(9):1051-8. DOI: 10.1001/archpsyc.1976.01770090041003. View
2.
DEMYER M, SHEA P, Hendrie H, Yoshimura N . Plasma tryptophan and five other amino acids in depressed and normal subjects. Arch Gen Psychiatry. 1981; 38(6):642-6. DOI: 10.1001/archpsyc.1981.01780310042003. View
3.
Stokes P, Stoll P, Koslow S, Maas J, Davis J, Swann A . Pretreatment DST and hypothalamic-pituitary-adrenocortical function in depressed patients and comparison groups. A multicenter study. Arch Gen Psychiatry. 1984; 41(3):257-67. DOI: 10.1001/archpsyc.1984.01790140047006. View
4.
Berger M, Doerr P, Lund R, Bronisch T, von Zerssen D . Neuroendocrinological and neurophysiological studies in major depressive disorders: are there biological markers for the endogenous subtype?. Biol Psychiatry. 1982; 17(11):1217-42. View
5.
Carroll B . The dexamethasone suppression test for melancholia. Br J Psychiatry. 1982; 140:292-304. DOI: 10.1192/bjp.140.3.292. View