Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression (2024)

Abstract

The autonomic nervous system is one of the major neural pathways activated by stress. In situations that are often associated with chronic stress, such as major depressive disorder, the sympathetic nervous system can be continuously activated without the normal counteraction of the parasympathetic nervous system. As a result, the immune system can be activated with increased levels of proinflammatory cytokines. These inflammatory conditions have been repeatedly observed in depression. In the search for the mechanism by which the immune system might contribute to depression, the enhanced activity of indoleamine 2,3-dioxygenase by pro-inflammatory cytokines has been suggested to play an important role. Indoleamine 2,3-dioxygenase is the first enzyme in the kynurenine pathway that converts tryptophan to kynurenine. Elevated activity of this enzyme can cause imbalances in downstream kynurenine metabolites. This imbalance can induce neurotoxic changes in the brain and create a vulnerable glial-neuronal network, which may render the brain susceptible to depression. This review focuses on the interaction between stress, the autonomic nervous system and the immune system which can cause imbalances in the kynurenine pathway, which may ultimately lead to major depressive disorder.

Original languageEnglish
Pages (from-to)665-673
Number of pages9
JournalCurrent Neuropharmacology
Volume14
Issue number7
DOIs
Publication statusPublished - 2016 Oct 1
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2016 Bentham Science Publishers.

Keywords

  • Autonomic nervous system
  • Immune system
  • Kynurenine pathway
  • Major depressive disorder
  • Stress

ASJC Scopus subject areas

  • Pharmacology
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Pharmacology (medical)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  • Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression (1)

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Won, E., & Kim, Y. K. (2016). Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression. Current Neuropharmacology, 14(7), 665-673. https://doi.org/10.2174/1570159X14666151208113006

Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression. / Won, Eunsoo; Kim, Yong Ku.
In: Current Neuropharmacology, Vol. 14, No. 7, 01.10.2016, p. 665-673.

Research output: Contribution to journalReview articlepeer-review

Won, E & Kim, YK 2016, 'Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression', Current Neuropharmacology, vol. 14, no. 7, pp. 665-673. https://doi.org/10.2174/1570159X14666151208113006

Won E, Kim YK. Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression. Current Neuropharmacology. 2016 Oct 1;14(7):665-673. doi: 10.2174/1570159X14666151208113006

Won, Eunsoo ; Kim, Yong Ku. / Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression. In: Current Neuropharmacology. 2016 ; Vol. 14, No. 7. pp. 665-673.

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abstract = "The autonomic nervous system is one of the major neural pathways activated by stress. In situations that are often associated with chronic stress, such as major depressive disorder, the sympathetic nervous system can be continuously activated without the normal counteraction of the parasympathetic nervous system. As a result, the immune system can be activated with increased levels of proinflammatory cytokines. These inflammatory conditions have been repeatedly observed in depression. In the search for the mechanism by which the immune system might contribute to depression, the enhanced activity of indoleamine 2,3-dioxygenase by pro-inflammatory cytokines has been suggested to play an important role. Indoleamine 2,3-dioxygenase is the first enzyme in the kynurenine pathway that converts tryptophan to kynurenine. Elevated activity of this enzyme can cause imbalances in downstream kynurenine metabolites. This imbalance can induce neurotoxic changes in the brain and create a vulnerable glial-neuronal network, which may render the brain susceptible to depression. This review focuses on the interaction between stress, the autonomic nervous system and the immune system which can cause imbalances in the kynurenine pathway, which may ultimately lead to major depressive disorder.",

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AB - The autonomic nervous system is one of the major neural pathways activated by stress. In situations that are often associated with chronic stress, such as major depressive disorder, the sympathetic nervous system can be continuously activated without the normal counteraction of the parasympathetic nervous system. As a result, the immune system can be activated with increased levels of proinflammatory cytokines. These inflammatory conditions have been repeatedly observed in depression. In the search for the mechanism by which the immune system might contribute to depression, the enhanced activity of indoleamine 2,3-dioxygenase by pro-inflammatory cytokines has been suggested to play an important role. Indoleamine 2,3-dioxygenase is the first enzyme in the kynurenine pathway that converts tryptophan to kynurenine. Elevated activity of this enzyme can cause imbalances in downstream kynurenine metabolites. This imbalance can induce neurotoxic changes in the brain and create a vulnerable glial-neuronal network, which may render the brain susceptible to depression. This review focuses on the interaction between stress, the autonomic nervous system and the immune system which can cause imbalances in the kynurenine pathway, which may ultimately lead to major depressive disorder.

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Stress, the autonomic nervous system, and the immune-kynurenine pathway in the etiology of depression (2024)

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