Abstract
Chronic inflammation in physically ill patients is often associated with the development of symptoms of depression. The mechanisms that are responsible for inflammation-associated depression have been elucidated over the last few years. Kynurenine produced from tryptophan in a reaction catabolized by indoleamine 2,3 dioxygenase is transported into the brain where it is metabolized by microglial enzymes into a number of neurotropic compounds including quinolinic acid, an agonist of N-methyl-d-aspartate receptors. Quinolinic acid can synergize with glutamate released by activated microglia. This chain of events opens the possibility to treat inflammation-induced depression using therapies that target the transport of kynurenine through the blood-brain barrier, the production of quinolinic acid and glutamate by activated microglia, or the efflux of glutamate from the brain to the blood.
Original language | English (US) |
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Pages (from-to) | 925-932 |
Number of pages | 8 |
Journal | Journal of Neural Transmission |
Volume | 121 |
Issue number | 8 |
DOIs | |
State | Published - Aug 2014 |
Keywords
- Depression
- Glutamate
- Inflammation
- Kynureninie
- Microglia
- Tryptophan
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Psychiatry and Mental health
- Biological Psychiatry