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J Neural Transm (Vienna). 2014 Aug;121(8):925-32. doi: 10.1007/s00702-014-1187-1. Epub 2014 Mar 15.

Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression?

Author information

1
Division of Internal Medicine, Department of Symptom Research, MD Anderson Cancer Center, 1400 Pressler Street, Houston, TX, 77030, USA, rdantzer@mdanderson.org.

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.

PMID:
24633997
PMCID:
PMC4134384
DOI:
10.1007/s00702-014-1187-1
[Indexed for MEDLINE]
Free PMC Article

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