Acute and Chronic Mental Stress Both Influence Levels of Neurotransmitter Precursor Amino Acids and Derived Biogenic Amines

• Main Authors: Katharina Hüfner, Matyas Galffy, Jonas Egeter, Johannes M. Giesinger, Kathrin Arnhard, Herbert Oberacher, Johanna M. Gostner, Dietmar Fuchs, Barbara Sperner-Unterweger
• Format: Article
• Language: English
• Published: MDPI AG 2020-05-01
• Series: Brain Sciences
• Subjects: phenylalanine; tyrosine; kynurenine; tryptophan; neurotransmitter precursor amino acids; mental stress
• Online Access: https://www.mdpi.com/2076-3425/10/6/322

Acute and chronic mental stress are both linked to somatic and psychiatric morbidity, however, the neurobiological pathways of these associations are still not fully elucidated. Mental stress is known to be immunomodulatory, which is one of the basic concepts of psychoneuroimmunology. In the present study, neurotransmitter precursor amino acid levels and derived biogenic amines were analyzed prior to and at 0, 30 and 60 minutes following an acute mental stress test (with/without chronic mental stress) in 53 healthy subjects. Psychometric measurements of mental stress, depression and anxiety were collected. Kynurenine/tryptophan was influenced by the factor acute mental stress (KYN/TRP increase), no influence of the factor chronic mental stress or any interaction was found. Phenylalanine/tyrosine was influenced by the factor acute mental stress (PHE/TYR increase) as well as by chronic mental stress (PHE/TYR decrease). Interactions were not significant. KYN/TRP correlated with state anxiety values, while PHE/TYR correlated negatively with chronic stress parameters. Kynurenic acid was significantly reduced in the acute and quinolinic acid in the chronic mental stress condition. In conclusion, neurotransmitter precursor amino acid levels and derived biogenic amines are influenced by acute and chronic mental stress. Mechanisms beyond direct immunological responses may be relevant for the modulation of neurotransmitter metabolism such as effects on enzyme function through cofactor availability or stress hormones.