期刊
JOURNAL OF NEURAL TRANSMISSION
卷 121, 期 8, 页码 925-932出版社
SPRINGER WIEN
DOI: 10.1007/s00702-014-1187-1
关键词
Inflammation; Depression; Glutamate; Tryptophan; Kynureninie; Microglia
资金
- University of Texas MD Anderson Cancer Center
- National Institute of Neurological Diseases and Stroke of the National Institutes of Health [R01 NS073939, R01 NS074999]
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.
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